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-DR. KAPIL ARORA NUTRITION AND PERIODONTIUM

Nutrition and periodontium

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  1. 1. -DR. KAPIL ARORA NUTRITION AND PERIODONTIUM
  2. 2. CONTENTS INTRODUCTION HISTORY LOCAL EFFECT OF DIET ON PERIODONTIUM INTERACTION OF IMMUNITY, INFECTION AND NUTRITIONAL STATUS NUTRITION AND PERIODONTAL HEALTH INTERRELATIONSHIP EFFECT OF DIFFERENT NUTRIENTS ON THE PERIODONTIUM PHYSICAL EFFECTS OF FOOD ON PERIODONTAL HEALTH DIET IN PERIODONTAL SURGERY CLINICAL AND LABORATARY ASSESSMENT ON NUTRITION STATUS IN DENTAL PRACTICE JOURNALS REVIEW CONCLUSION
  3. 3. The knowledge of food and nutrition has a direct bearing on the maintenance of sound health of an individual.
  4. 4. NUTRITION W.H.O: the science of food and its relationship to health. It is concerned primarily with the part played by the nutrient in body growth, development and maintenance. NIZEL: the science which deals with the study of nutrients and foods and their effects on the nature and function of the organism under different conditions of age, health and disease. DCNA 2003: the science, how the body utilizes food to meet the requirement for development , growth, repair and maintenance.
  5. 5. MACRONUTRIENTS MICRONUTRIENTS CARBOHYDRATES PROTEINS FATS VITAMINS MINERALS
  6. 6. The majority of opinions and research findings on the effects of nutrition on oral and periodontal tissues point to the following: THERE ARE NUTRITIONAL DEFICIENCIES THAT PRODUCE CHANGES IN ORAL CAVITY. THERE ARE NO NUTRITIONAL DEFICIENCIES THAT BY THEMSELVES CAN CAUSE GINGIVITIS OR PERIODONTAL POCKETS. PHYSICAL CHARACTER OF THE DIET
  7. 7. The study of the teeth and supporting structures of ancient populations provides some useful information about the effect of diet, and in particular its consistency. on rates of dental attrition and the progression of periodontal disease. Populations such as the Egyptians who had severe attrition from a very coarse diet, there was a greater prevalence of periodontal disease than caries (Deeley 1976).
  8. 8. A study of dental disease in the Natufians at Kebara in Israel found a low rate of attrision with little calculus and periodontal disease (Smith 1972). This type of disease is more typical of hunting-based populations eating non-abrasive but self-cleansing diet based predominantly on meat rather than on cereals and vegetables alone A study by Clark et al (1986) showed that in many premodern population the evidence of periodontal disease was less. 90 % of teeth examined showed no discernible bone loss despite the presence of large deposits of calculus
  9. 9. LOCAL EFFECT OF DIET ON PERIODONTAL HEALTH
  10. 10. Vigorous masticatory function is associated with a widening of the PDL (Collidge 1937) Aukes et al (1987) suggest that chewing pattern depends on the texture of the masticated food , hard and tough food requiring more vertical movements and soft food requiring less vertical movement.
  11. 11. INTERACTION OF IMMUNITY, INFECTION AND NUTRITIONAL STATUS Nutrition is a critical determinant of immune responses. (R.K.Chandra.Am J clin Nutrition 1991) Due to the fact that nutrients derived from food sources such as proteins, carbohydrates and fats as well as micronutrients vitamins and minerals interact with immune cells in the blood streams, lymph nodes and specialized immune system of the gastrointestinal tract. (Cunningham-Rundles S .Nutr Rev 1998)
  12. 12. Infections no matter how mild have adverse effects on nutritional status. Majority of nutrient deficiencies will impair the immune response and predispose the individual to infection. Scrimshaw NS,San Giovanni JP.Am J Clin Nutr 1997 Individuals who are undernourished have impaired immune response including abnormality in adaptive immunity , phagocytosis and antibody function R.K.Chandra.Am J clin Nutrition 1991 Epidemiological and clinical data also suggests that nutritional deficiencies alter immune responses and increase the risk of infection R.K.Chandra.Am J clin Nutrition 1997
  13. 13. Nutrition and Periodontal health interrelationship
  14. 14. Loss of connective tissue attachment evident during active periodontal disease is a result of basic interaction between virulence of the infecting organisms and the resistance of the host
  15. 15. This destruction is a consequence of infection. and a nutritional deficiency alone is no longer believed to initiate periodontal disease, it is more likely, that a state of malnutrition will predispose a subject to onset of a periodontal infection, or will modify the rate of progression of established disease (Glickman 1964) (Ferguson 1969)
  16. 16. Food and nutrition affect periodontal health at 3 levels Contributing to microbial growth in gingival crevice Affecting the immunological response to bacterial antigen Assisting in the repair of connective tissue at the local site after injury from plaque calculus and so forth
  17. 17. NUTRITION AND EPITHELIAL BARRIER Rapid rate of turn over of epithelial cells of gingival sulcus indicates the need of continuous synthesis of DNA, RNA and tissue protein This indicates that sulcular epithelium has high requirement of such nutrients as folic acid and protein which are involved in cell formation At the base of the sulcular epithelium is a narrow basement membrane made up of collagen Since collagen is the major component of basement membrane and ascorbic acid and zinc are important for collagen synthesis This membrane act as a barrier for entrance of toxic material
  18. 18. THE EFFECT OF NUTRITION UPON ORAL MICROORGANISMS. Although dietary intake is generally thought of in terms of sustaining the individual it also source of bacterial nutrients. Composition of the diet may influence the relative distribution of types of microorganism their metabolic activity, their pathogenic potential which in turn affects the occurrence and severity of oral disease. Morhant & Fitzgerald 1976
  19. 19. HOST NUTRITION AND PLAQUE BIOFILM Nutrition has both direct and indirect effects on development and composition of plaque biofilm The biofilm is made up primarily of microorganisms that include bacteria. Fungi, yeasts. and viruses In addition, 20 to 3O% of the plaque mass is made up of intracellular matrix consisting of organic and inorganic components The organic components include polysaccharides, proteins, glycoproteins and lipids. Inorganic components are primarily calcium and phosphorus with trace amounts of sodium, potassium and fluoride
  20. 20. The early bacteria colonizing the dental pellicle are aerobic, gram-positive and primarily use sugars as an energy source The secondary colonizers of the more mature plaque biofilm are anaerobic, gram negative bacteria and use amino acids and small peptides as energy sources The primary mechanism by which nutrition impacts the biofilm is through a direct supply or specific nutrients (such as sucrose) as substrates for energy, nitrogen, or carbon for the bacteria. An example of this is the introduction of excess glucose to a plaque biofilm which has been shown to result in an increased rate of bacterial growth in the early stages of biofilm development
  21. 21. For example, the growth of Porphyromonas gingivalis is facilitated by the metabolic by- product succinate from organisms like Compylobacter rectus The organisms colonizing the biofilm tend to form complexes that are mutually supportive of each others growth.
  22. 22. The third mechanism by which nutrition effects biofilm is through the production of specific polymers used by bacteria. Eg-use of sucrose to produce the glycans used to facilitate adherance of bacteria such as streptoccoccus mutans to the dental pellicle
  23. 23. PROTEINS Proteins are complex organic nitrogenous compounds. They are indispensable, constituents of the diet because they are the only source of the amino-acids including the essential amino-acids; these are: valine, lysine, leucine, isoleucine, methionine, tryptophan, threonine histidine,phenylalanine.
  24. 24. SOURCES
  25. 25. PROTEINS AND DENTAL TISSUES
  26. 26. FATS AND LIPIDS
  27. 27. SOURCES
  28. 28. CARBOHYDRATES
  29. 29. SOURCES Sources (a) Starches: these are 'complete sugar', present in abundance in cereals and millets roots and tubers. (b) Sugars: monosaccharides e.g. glucose, fructose, galactose, disaccharides e.g., sucrose, lactose and maltose. (c) Cellulose or dietary fibre: This is the fibrous substance lining fruits, vegetables and cereals. It is the indigestible component of carbohydrate with hardly any nutritive value.
  30. 30. DAILY REQUIREMENTS
  31. 31. EFFECT ON THE PERIODONTIU M
  32. 32. VITAMINS Vitamins can be defined as naturally occurring organic substances which are required in minute amount to maintain normal health of the organism and which have to be supplied in food as they cannot be synthesized by the organism
  33. 33. VITAMIN A MCCOLLUM is credited with the discovery of this vitamin. He gave the name FAT SOLUBLE A to the substance.
  34. 34. REQUIREMENTS: (WHO 1967) 750 microgram (2500 IU) or 3000 micrograms (5000 IU) of beta carotene for an adult. Pregnant and Lactating women have to be provided 50% more.
  35. 35. VITAMIN-A DEFICIENCY AND PERIODONTAL DISEASE Gingival hyperplasia with inflammation infiltrate, pocket and suggingival calculus MARSHALL DAY reported a possible correlation between the incidence of periodontal disease and dermatological lesions characteristic of vit A deficiency and RUSSELL reported that populations with a high incidence of periodontal disease tend to be deficient in vit-A T/t-Single large dose of 60mg retinol as given orally. If there is vomiting or diarrhea 55mg retinol IM injection is recommended.
  36. 36. HYPERVITAMINOSIS- A Gingival erosions and ulcerations, loss of keratinization and desquamation of lips were reported in one human case. Melanin like pigmentation of skin, scaling dermatosis, disturbed menstruation, itching, and exophthalmos have been identified with hypervitaminosis in humans.
  37. 37. VITAMIN D ANGUS, WINDUS TYPES: I. Vit D1- that is not sufficiently active II. Vit D2-obtained by irradiating (with U.V light) the plant sterol ergosterol III. Vit D3- formed by irradiating animal ergosterol
  38. 38. WHY DO WE NEED VIT D?? Vit D promotes absorption of calcium & phosphorus. Vit D promotes growth in general. It facilitates the normal functioning of parathormone. It promotes mineralization of bone. It is some times used in the treatment of tetany. It some how acidifies the PH of distal ileum, colon and caecum. It increases citrate content of bone, blood and other tissues. It exerts an antirachitic effect.
  39. 39. The national research council (USA 1964) recommended intake of 400 IU/day for infants and growing children. In tropical countries with plenty of sunlight, smaller amounts may be sufficient. The nutritional expert group India recommended a daily supply of 200 IU.
  40. 40. VITAMIN-D DEFICIENCY AND PERIODONTAL DISEASE ENAMEL HYPOPLASIA A small number of patients with evidence of rickets develop enamel hypoplasia. Whether these teeth are more susceptible tooth dental caries is uncertain. The enamel does not appear to be weakened, but the rougher surface may facilitate adherence of dental plaque and food residue. In severe cases of Vit-D deficiency, a calcitraumatic line may develop. [SWEENEY AND SHAW 1988].
  41. 41. HYPERVITAMINOSIS- D The periodontal findings in experimental Hypervitaminosis D include osteosclerosis characterized by marked defects in the endosteal and periosteal bone formation. Osteoporosis and resorption of alveolar bone, dystrophic calcification in the periodontal ligaments and gingiva, severe calculus formation, deposition of a cementum like substance on the root surfaces [hypercementosis and the ankylosis of many teeth] and extensive periodontal disease.
  42. 42. VITAMIN- E In 1922 BISHOP and EVANS termed the food factor as FACTORX which was subsequently renamed as Vit E.
  43. 43. Average human diets contain about 30 IU [20mg] of D alfatocopherol and since no deficiency is ever reported, this is considered as adequate amount
  44. 44. HYPER AND HYPO STATES Oral Vit E supplementation results in few side effects even at doses as high as 3200mg/day [BENDICH and MACHLIN 1988]. Favorable response to Vit E therapy has been reported in patients with severe periodontal disease with a minimum of local factors.
  45. 45. VITAMIN K DAM (1935) named the factor present in natural diets and which protected against the hemorrhagic disease as Vit K (koagulation Vitamin). DAM and KARRER in 1939 isolated the vitamin as crystalline form. K1 (phylloquinone) which occurs in green plants, and K2 (menaquinone) which is formed by Escherichia coli bacteria in the large intestine and is found in animal tissues and the fat soluble synthetic compound menadione (K3).
  46. 46. FUNCTIONS
  47. 47. REQUIREMENTS The RDA for adult men is 80mcg and for women 65mcg with the exception of females between 25 30 years of age. (BOOTH et al 1996)
  48. 48. SOURCES Green leafy vegetables are high in Vit -K, but meat and dairy products provide significant amounts. Bacterial flora in the jejunum and ileum synthesize Vit K.
  49. 49. VITAMIN K DEFICIENCY 100mg IM for 3 5 days.
  50. 50. VITAMIN C Scurvy was known for centuries. Lind gave accurate description of the disease as early as 1757. Gyorgi in 1928 isolated a substance from adrenal gland called hexuronic acid, which was later identified as Vit C by Waugh and king (1932).
  51. 51. SOURCES
  52. 52. REQUIREMENTS 30mg for infants and 70mg for adults are recommended by NRC (National Research Council). More is required during pregnancy and lactation. The nutritional expert group (ICMR) has recommended 50mg/day as adequate for Indians.
  53. 53. SCURVY Hemorrhagic lesions into the muscles of the extremities, the joints, sometimes nail beds, petechial hemorrhage often seen around hair follicles. Increased susceptibility to infections, impaired wound healing, bleeding and swollen gingiva loosened teeth, defective formation and maintenance of collagen, retardation or cessation of osteoid formation, impaired osteoblastic activity and increased capillary permeability are most common. Susceptibility to traumatic hemorrhages, hyporeactivity of the contractile elements of the peripheral blood vessels is also seen.
  54. 54. POSSIBLE ETIOLOGICAL RELATIONSHIPS BETWEEN ASCORBIC ACID AND PERIODONTAL DISEASE Low levels of ascorbic acid influences the metabolism of collagen with in periodontium, there by affecting the ability of the tissues to regenerate and repair it self. Ascorbic acid deficiency interferes with bone formation, leading to loss of periodontal bone (failure of osteoblast to form osteoid). Ascorbic acid deficiency increases the permeability of the oral mucosa to tritiated endotoxin and tritiated inulin and of normal human crevicular epithelium to tritiated dextran. Increase in levels of ascorbic acid enhances both the chemotactic and migratory action of leukocytes with out influencing their phagocytotic activity. An optimal level of ascorbic acid is apparently required to maintain the integrity of the periodontal vasculature, as well as the vascular response to bacterial irritation and around healing Depletion of Vit C may interfere with the ecological equilibrium of bacteria in plaque and thus increase its pathogenicity.
  55. 55. GINGIVITIS Enlarged, hemorrhagic, bluish red gingiva is described. Gingivitis in Vit C deficiency patient is caused by bacterial plaque. Vit C deficiency may aggravate the gingival response to plaque and worsen the edema, enlargement and bleeding. Correcting the deficiency may decrease the severity of the disorder. Gingivitis will remain as long as bacterial plaque factors are present.
  56. 56. PERIODONTITIS Edema, hemorrhage in the periodontal ligament Osteoporosis of alveolar bone, Tooth mobility and degeneration, Hemorrhage edema and degeneration of collagen fibers, Retards gingival healing, Periodontal fibers present below the junctional epithelium and above the alveolar crest are least affected. (Explains the infrequent apical down growth of the epithelium).
  57. 57. Vit C deficiency does not cause periodontal pockets. Local bacterial factors are required for pocket formation to occur. Vit C deficiency accentuates destruction of the periodontal ligament and alveolar bone. This is due to inability to marshal a defensive delimiting connective tissue barrier reaction to the inflammation and partly from destructive tendencies of fibroblast formation and differentiation to osteoblasts, as well as impaired formation of collagen and mucopolysaccharide ground substance. (A case reported by Charbeneau and Hurt showed worsening of a preexisting moderate periodontitis with development of scurvy) Vit C deficiency has its greatest impact on periodontal disease when preexisting disease and other co destructive factors are present. 100mg Vit C TID
  58. 58. B COMPLEX GROUP OF VITAMINS It is the anti beriberi factor present in rice polishing, yeast and liver. It was originally called the water soluble Vit B to distinguish it from fat-soluble - A known of the time of 1920s. In course of time several water-soluble factors acting as vitamins were found to be the same sources like rice polishing, yeast and liver and these were named B1, B2 etc. Subsequently their normal structure was identified and they were assigned more rational names based on their chemistry. Some of them are synthesized in the tissues of the higher animals, and so do not strictly satisfy the definition of vitamin.
  59. 59. SOURCES Generally they are rich in germinating seeds, rice polishing, wheat germ, pulses, beans and lentils, yeast, liver and meat.
  60. 60. THIAMINE (VIT B1: ANTI BERIBERI SUBSTANCE; ANTINEURITIC VITAMIN; ANEURINE) REQUIREMENTS They depend mainly upon, caloric intake and particularly carbohydrate intake of the individual. For a adult taking 3000 calories/day. 1.5mg of thiamin is required. ORAL DISTURBANCES Hypersensitivity to oral mucosa, minute vesicles (simulating herpes) on the buccal mucosa, under the tongue or in the palate and erosion of the oral mucosa. TREATMENT 50mg thiamin for the first 3 days and 10mg 3 times a day should be continued there after by mouth until convalescence is established.
  61. 61. RIBOFLAVIN ( VIT B2, LACTOFLAVIN) SOURCES Milk, liver, kidney, heart, egg yolk and germinating seed. Riboflavin is destroyed on exposure to light and is reduced to colorless products. REQUIERMENTS 1.5 to 2.0 mg/day NEG, India, has recommended an intake of 0.55mg/1000 calories, some as that recommended by WHO group. DEFICIENCY Glossitis Angular chelitis. Seborrheic dermatitis. Superficial vascularized keratosis. TREATMENT 5 mg 3 times a day.
  62. 62. NIACIN (P-P FACTOR, PELLAGRA PREVENTING FACTOR OF GOLD BERGER, NICOTINIC ACID) Gold burger (1912) identified pellagra as a disease caused by deficiency of dietary factor. Elevehjem in 1937 isolated nicotinic acid and its amide from liver extract and showed its efficiency in curing these conditions.
  63. 63. REQUIREMENTS National Research Council, U.S.A recommended 6.6mg/1000 calories (FAO/WHO group). Nutrition Expert Group for Indian conditions also confirmed this. For a 3000 calories diet, this works out 20mg/day. ORAL SYMPTOMS Glossitis Gingivitis Generalized stomatitis. TREATMENT 100mg every 6 hours, smaller dose are likely to be effective. Well absorbed parentally.
  64. 64. FOLIC ACID SOURCES Green leafy vegetables are good sources besides usual sources of B Complex. REQUIREMENTS 300 to 500 micrograms are adequate to maintain normal health. The nutrition expert group (ICMR) recommends 100micrograms/day for an adult. Oral changes like generalized stomatitis, Ulcerated glossitis and Chelitis.
  65. 65. PYRIDOXINE REQUIREMENTS : - 2mg a day for adults ORAL CHANGES IN HUMANS Angular chelitis glossitis with swelling atrophy of the papillae, magenta discoloration and discomfort. TREATMENT 30 mg as supplementation dose per day, 100mg per day is required in penicillamine therapy.
  66. 66. MINERALS (1) The body contains some 50 minerals which serve specific functions in the body. The mineral constituents of the body amount to 4.3- 4.4% largely in the skeleton (2) The important minerals include: Calcium, phosphorus, iron, sodium, potassium and magnesium
  67. 67. COPPER A positive and significant correlation has been demonstrated between serum copper and the severity of periodontal disease (Freeland et al 1976). The inflammatory process itself is known to elevate serum copper (Gubler et al 1958) Copper is also essential for the development and maturation of connective tissues (ODell etal 1961). A copper metalloenzyme contributes to the stabilization of collagen (Burch et al 1975).
  68. 68. Freeland etal (1976) suggested that if this enzyme accumulates in blood or if copper is not transferred to the periodontal tissues then a elevaton in serum levels of copper will occur.
  69. 69. ZINC Zinc levels in serum have also been studied and found to decrease with an increase in alveolar bone resorption Periodontal Zinc levels in serum have also been studied and found to decrease with an increase in alveolar bone resorption (Frithiof et al 1980). Zinc can inhibit several functions of polymorphonuclear leukocytes (Chapvil el of 1977)
  70. 70. The ions also stabilize the cell membranes and inhibit the release of lysosome enzymes (Chapvil 1973). Reduction in serum zinc in periodontal disease, therefore may stimulate both leukocyte function and the release of potent enzymes that will enhance the inflammatory process and lead to loss of periodontal collagen.
  71. 71. Not all workers have detected variations in levels of trace elements in periodontal disease. Kilgore et al. (1969) failed to find a relationship between serum levels of and periodontal status.
  72. 72. FLUORIDE FUNCTIONS: Incorporated into tooth structure Aids in resistance to caries Excess: Disturbed amelogenesis Mottled enamel
  73. 73. CALCIUM SOURCES: Milk & milk products Eggs ABSORPTION: principally upper part jejunum Other parts of the intestine as well.
  74. 74. DEFICIENCY: Incomplete mineralization of teeth Excessive bone resorption and bone fragility Increased tendency to haemorrhage Increased tooth mobility Premature tooth loss PEAK BONE MASS Osteoporosis
  75. 75. CALCIUM AND PERIODONTIUM The cardinal sign of periodontal disease is loss of connective tissue attachment including the resorption of alveolar bone In periodontal ligament the number and diameter of dentoalveolar fibers were reduced this may have resulted from alteration in the masticatory activity due to loss of mineralised tissue
  76. 76. Some reports indicate a correlation between bone health and periodontal diseases. Klemettie and collaborators concluded from their study of 227 healthy postmenopausal women, aged 48 to 56 years, that individuals with high mineral content of their bone seemed to retain teeth with deep periodontal pockets more easily than those who had osteoporosis ( DCNA Vol 47 April 2003)
  77. 77. Several Findings suggest that whereas a hypocalcaemic diet can produce interradicular alveolar osteoporosis and thinning of individual trabeculae. it will not initiate inflammation, migration of the epithelial attachment, loss of periodontal fibers or resorption of the alveolar margin (Svanberg et aL. 1973; Bissada and DeMarco 1974).
  78. 78. The evidence implicating the importance of calcium in human periodontal disease is even more equivocal. Lutwak et al (1971) found that daily supplements with calcium (100mg/day) decreased gingivitis, pocket depths, and tooth mobility in an uncontrolled study of 10 patients. Further in a controlled and cross-over radiographic study they also reported an increase in density of alveolar bone in patients receiving 1000 mg daily supplements for six months (Lutwak et aL 1971).
  79. 79. Baer (1977), however, proposes that calcium does not play a significant role in the initiation or progression of periodontal disease and that the most important factor is the interaction between plaque and the hosts immune response
  80. 80. PHYSICAL EFFECTS OF FOOD ON PERIODONTAL HEALTH
  81. 81. normal growth and development of periodontal and oral mucosal tissues Vit A (salivary glands, epithelial tissue) Vit C (Collagen, Connective tissue), and Vit B Complex (epithelial, connective tissue). Calcification of the alveolus and cementum amino acids, calcium, and phosphorus, Vit - D and magnesium. Maintenance of oral tissues, as well as the integrity of hosts immune and repair response Vit A, C, D, Protein, Carbohydrates, Calcium, Iron, Zinc and Folic acid
  82. 82. FOOD CONSISTENCY Chewing firm, coarse and fibrous foods such as raw fruits and vegetables will stimulate salivary flow. The increase in saliva will enhance oral clearance of food, there by reduction in food retention. Nizel and papas (1989) reported that mastication of firm, fibrous foods can also stimulate and strengthen the periodontal ligament and perhaps may also increase the density of alveolar bone adjacent to the roots.
  83. 83. DIET IN PERIODONTAL SURGERY
  84. 84. PRE-OPERATIVE Periodontal surgery and healthy patients with an adequate in take dont require special dietary modification. Surgery on a chronic alcoholic would most likely require preoperative replenishment of several nutrient deficiencies. Recommendation of a liquid nutritional supplements or multivitamins may be warranted. Surgery may be postponed for one to two weeks to allow nutritional status to improve.
  85. 85. POST-OPERATIVE The requirements for calories, protein, vitamins, minerals and water may be double the speed recovery time (Nizel and papas 1989), liquid diet may be required for the first one to two days. This can be progressed in to a mechanical soft diet after one to two days for 3 to 5 days. A liquid supplements and is a multivitamin may be recommended to ensure adequate nutrition and to shorten duration of recovery.
  86. 86. NUTRITION ORAL HEALTH
  87. 87. NUTRITION-RISK SCREENS Nutritional risk factors are defined as characteristics that are associated with an increased likelihood of poor nutritional status
  88. 88. TABLE OUTLINES NORMAL VALUES AND THEIR INTERPRETATION FOR THE COMPLETE BLOOD COUNT
  89. 89. JOURNALS REVIEW
  90. 90. The affect of calcium and periodontal disease are likely related to alveolar bone. Change which eventually results in greater clinical attachment loss. J.Periodontal 2000, 71, 1057 1066 (by Mieko Nishida et al) Vit C known as one of the powerful scavenger of super oxide anions, smokers, may need more antioxidants to prevent the harmful influences of tobacco products on periodontal tissue. Low levels of dietary Vit C were associated with more severe periodontal disease in tobacco users but not in non-tobacco users. J.Periodontal 2000, 71,1215 1223 (by Mieko Nishida et al) In vitro treatment with ascorbate containing Vit-C metabolites enhanced the formation of mineralized nodules and collagenous proteins. J.Periodontal 1999,70,992 999 (by Dorothy J Rowe et al)
  91. 91. Osteoporosis is multifactorial and genetic factor plays an important role. The polymorphism in Vit D Receptor gene is linked to decrease bone mass in postmenopausal women. Genes and Osteoporosis 1997; 8; 232 286 [STRUAN et al] Even in the continuing presence of plaque, gingival health can be significantly enhanced by improved nutrient intake suggests important implications for the maintenance care of marginally deficient individual. J.Periodontal; 1985;56;558 561 [By Barry Webb Jones, et al)