this presentation is on the relationship and effect of nutrition on general and oral health management of few cases and pictures of the same are also included

1. -DR. KAPIL ARORA
NUTRITION AND PERIODONTIUM

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. The knowledge of food and
nutrition has a direct
bearing on the
maintenance of sound
health of an individual.

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. MACRONUTRIENTS MICRONUTRIENTS
CARBOHYDRATES
PROTEINS
FATS
VITAMINS
MINERALS

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. • 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. • 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. LOCAL EFFECT
OF DIET ON
PERIODONTAL
HEALTH

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. 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. 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. Nutrition and Periodontal
health interrelationship

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. 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. 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

18. 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

19. 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

20. 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

21. 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

23. 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.

24. 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

26. 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.

28. SOURCES

30. PROTEINS AND DENTAL TISSUES

33. FATS AND LIPIDS

36. SOURCES

38. CARBOHYDRATES

39. 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.

40. DAILY REQUIREMENTS

41. EFFECT ON
THE
PERIODONTIU
M

42. 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

43. VITAMIN A
• MCCOLLUM is credited with the discovery of this vitamin. He gave the name “FAT
SOLUBLE A” to the substance.

44. • 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.

45. 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.

46. 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.

47. 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

48. 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.

49. • 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.

50. 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].

51. 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.

52. VITAMIN- E
• In 1922 BISHOP and EVANS termed the food factor as FACTOR’X’ which
was subsequently renamed as Vit – E.

53. • Average human diets contain
about 30 IU [20mg] of D –
alfatocopherol and since no
deficiency is ever reported, this
is considered as adequate
amount

54. 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.

55. 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).

56. FUNCTIONS

57. 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)

58. 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.

59. VITAMIN K DEFICIENCY
100mg IM for 3 – 5 days.

60. 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).

61. SOURCES

62. 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.

63. 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.

64. 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.

65. 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.

66. 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).

67. • 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

68. 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.

69. SOURCES
Generally they are rich in
germinating seeds, rice
polishing, wheat germ,
pulses, beans and lentils,
yeast, liver and meat.

70. 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.

71. 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.

72. 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.

73. 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.

74. 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.

75. 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.

76. 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

77. 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
(O’Dell etal 1961).
A copper metalloenzyme contributes to the
stabilization of collagen
(Burch et al 1975).

78. 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.

79. 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)

80. 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.

81. 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.

82. FLUORIDE
FUNCTIONS:
Incorporated into tooth structure
Aids in resistance to caries
Excess:
Disturbed amelogenesis
Mottled enamel

85. CALCIUM
SOURCES:
Milk & milk products
Eggs
ABSORPTION:
principally – upper part jejunum
Other parts of the intestine as well.

86. 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

87. 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

88. 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)

89. • 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).

90. 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).

91. 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
host’s immune response

92. PHYSICAL EFFECTS OF
FOOD ON PERIODONTAL
HEALTH

93. 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

94. 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.

95. DIET IN PERIODONTAL
SURGERY

96. PRE-OPERATIVE
Periodontal surgery and healthy patients with an adequate in take
don’t 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.

97. 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.

99. NUTRITION ORAL
HEALTH

100. NUTRITION-RISK SCREENS
Nutritional risk factors
are defined as
‘‘characteristics that
are associated with an
increased likelihood of
poor nutritional status

102. TABLE OUTLINES NORMAL VALUES AND THEIR
INTERPRETATION FOR THE COMPLETE BLOOD
COUNT

104. JOURNALS REVIEW

105. • 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)

106. • 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)