This document discusses the role of vitamins and minerals in periodontal health. It begins by introducing the topic and explaining the interaction between nutritional status and the immune response to bacteria in periodontal disease. It then discusses how various nutrients like carbohydrates, proteins, fats, vitamins and minerals can impact periodontal health and the host response if deficient. Specific vitamins and minerals are explained in depth, covering their sources, functions, effects of deficiencies, and relevance to periodontal tissues and immune response. The document provides an overview of how nutrition and nutritional deficiencies can influence periodontal disease development and progression.
2. Role of Vitamins and
Minerals in Periodontal
health
Presented by- Dr.Prerna Shirke
Guided by- Dr.Abhay Kolte
3. Introduction
▪ Comprehensive dental care requires dental professionals
to assess the general health of their patients and to
understand the implications of underlying factors that
may impact oral health.
▪ One of these underlying factors is the interaction between
nutritional status and the immune response to the
bacterial challenge in periodontal disease.
4. • Deterioration of oral health is highly correlated with deterioration
of general health, making it essential that the patient be well
nourished in order to respond to the challenge of infectious
disease like periodontal diseases.
• Although dental plaque is the major etiologic factor in periodontal
disease, inadequate nutrition may alter the host response to
bacterial irritants and render the host more susceptible to
establishment or progression of periodontal disease.
5. • Nutritional disorders may arise due to :
•Inadequate dietary intake.
•Disturbances in the absorption of nutrients.
•Economic and educational limitations.
•Self-imposed dietary restrictions.
•Geographic isolation from adequate food supply.
6. • Alfano (1976) suggested the following factors affected in nutritional
deficiencies:
•Protein and urea contents of both saliva and crevicular fluid.
•Integrity of the dentogingival barrier and the turnover of its
constituent cells.
•Mobilization and activation of PMNs in the early inflammatory
response.
•Activation of lymphocytes and the production of immunoglobulins
in the immune response.
7. Host nutrition and plaque biofilm
•Nutrition has both direct and indirect effects on the development
and composition of plaque biofilm.
•The primary mechanism by which nutrition impacts the
biofilm is through a direct supply of 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.
8. •The second mechanism by which nutrition has an (indirect)
impact on plaque biofilm is by having an effect on the production
of metabolic byproducts from one organism that provide
nutrients for other organisms.
•These by-products include lactate and formate from
Streptococcus and Actinomyces species, which are used as
nutrients by other bacteria.
9. •The third mechanism by which nutrition impacts the biofilm is
through the production of specific polymers used by other
bacteria.
•An example of this is the use of sucrose to produce the
glucans used to facilitate the adherence of bacteria such as
Streptococcus mutans to the dental pellicle.
•Glucose and other carbohydrates are also used to produce
extracellular polysaccharides and, therefore, diets containing
sucrose, glucose, and other disaccharides can increase the plaque
mass and facilitate the retention and colonization of the plaque
biofilm.
10. •Finally, nutrition impacts the plaque biofilm indirectly through by-
products of bacterial metabolism of a nutrient to alter the
environment of the biofilm and thereby influence the bacteria
colonizing the biofilm.
•As a by-product of the metabolism of sucrose and glucose,
bacteria produce acids that lower the pH, resulting in a more
favorable environment for the development of certain bacteria
such as S. mutans.
14. CARBOHYDRATES AND PERIODONTIUM
• Ground substance of gingival CT – proteoglycans (hyaluronic acid &
chondroitin sulphate) and glycoproteins (fibronectin & laminin).
• GCF - glucose hexosamine & hexuronic acid. Glucose concentration
is 3-4 times greater than that of serum.
• Ground substance of PDL – glycosaminoglycans (hyaluronic acid)
and proteoglycans and glycoproteins.
15. • Basement membrane – proteoglycans such as decorin, biglycan,
versican and syndecan.
• Active tricarboxylic cycle occurs in basal and suprabasal cells, where
proximity of the blood supply facilitates energy production through
aerobic glycolysis.
• Glycogen concentration is inversly related to the degree of
keratinization
16. ▪ Some findings exists suggesting that refined carbohydrates in diet
influence the severity of chronic inflammatory pd disease in humans
– Holloway et al 1963
▪ Poor glycemic control is known as an established risk factor of
periodontitis – Nishimura et al 1998
▪ Some evidence says that severe periodontal disease may deteriote
glycemic control – Taylor et al 1996
19. LIPIDS AND PERIODONTIUM
▪ Lipids form substances essential for maintaining cellular integrity
such as lipoproteins and glycolipids, in combination with proteins
and carbohydrates respectively.
▪ It is probable that essential fatty acid deficiency leads to reduction in
prostaglandins and leukotrienes, increasing the possibility of Pd
changes. These changes would be due, in part, to altered
inflammatory reaction – El-Atter et al 1978
▪ It is suggested that an inability to utilize particular fatty acids affects
fibroblast function in the metabolism of particular prostaglandins –
Emami et al 1992.
22. Proteins and Periodontium
▪ Proteins are the constituents of organic matrices of all the dental
tissues including alveolar bone and periodontal ligament. The
integrity of the periodontal ligament, the fibers of which are
remodelled constantly is dependent on a protein supply.
▪ dystrophic changes in the periodontal ligament, decreased
cementum formation, osteoporosis, resorption of the alveolar
bone and marked degeneration of periodontal support occur in
protein deprivation.
▪ Studies on the effects of protein supplements on the periodontal
structures in humans by Ringsdorf and Cheraskin in 1960s
revealed that a high – protein and low- carbohydrate diet had a
significant effect in reducing mobility, sulcus depth and in improving
gingival health.
23. • Mild PEM may impair the acute-phase response to infection
resulting in reduced host ability to mount an effective
inflammatory response to the invading pathogens.
• Although leukocytes are still able to phagocytize bacteria, they
are less effective at the subsequent intracellular destruction
of the bacteria.
• The lysozyme concentrations of saliva are also decreased as
a result of a reduction in production by monocytes and
neutrophils.
• Decrease in the amount of immunoglobulin secreted, such as
IgA by the saliva
• Bacterial adhesion to epithelial cells appears to be increased
in PEM thereby increasing the risk of invasion and infection
25. VITAMIN A
(RETINOL,RETINAL,RETINOIC ACID)
Dietary sources
Fish
oil,liver,other
organ
meats,yellow-
orange pigment
fruits and
vegetables and
green leafy
vegetables
Functions
Vision
Reproduction
Growth and
embryonic
development
Immune
functions
Deficiency
Nyctalopia,
xeropthalmia
(bitot’s spots),
keratomalacia,
follicular
hyperkeratosis
Hypervitaminosis
Bone and joint pain
Hair loss dryness and
fissures of the lips
anorexia weight loss
hepatomegaly
Low vitamin A
intake
associated with
periodontal
disease
Radusch et al
26. VITAMIN D
Sources
Fortified milk,fish liver
oils,exposure to
ultraviolet sun rays
Functions
Absorption of calcium
Bone metabolism
Deficiency
Rickets in children
Ostomalacia in adults
Osteodystrophy in renal
disease
Incomplete calcification
of teeth
Excess
Can be toxic
Leads to pulp
calcification and enamel
hypolplasia
27. Vitamin E(Tocopherols)
Sources
Cotton seed oil, sunflower
oil,wheat germ
oil,margarine,soya bean,
cabbage,yeast
Functions
Antioxidant
Reproduction and sterility
Cellular respiration
Synthesis of heme
Deficiency
Sterility
Muscular dystrophy
Hemolytic anemia
Depressed tendon
reflexs,ataxia and dysarthtria
Short life of rbc
29. VITAMIN C
(ASCORBIC ACID)
SOURCES
CITRUS
FRUITS,SPINACH,RADDIS
H TOMATOES
CELLULAR OXIDATION-
REDUCTION
COLLAGEN SYNTHESIS
TRYPTOPHAN,
CHOLESTROL AND
TYROSINE METABOLISM
FERRITIN FORMATION
AND IRON ABSORPTION
ELECTRON TRANSPORT
CHAIN
IMMUNOLOGICAL
FUNCTIONS
SPARING ACTION OF
OTHER VITAMINS
DEFICIENCY
SCURVY
FUNCTIONS
30. Clinical features of scurvy:
▪ Signs – Petechiae, ecchymoses and spontaneous bruising of the extremities.
▪ Haematuria, epistaxis, bleeding into the tissues, joints and muscles occur.
▪ Vascular congestion in the hair follicles leads to enlargement, keratosis and a
localized reddening of the skin.
▪ Hemorrhages in the subperiosteal region of long bones cause severe pain and
tenderness.
▪ Anemia may result from blood loss.
▪ Generalized lethargy and increased susceptibility to infections.
▪ Wound healing is delayed particularly in deeper layers that rely on capillary
growth and the production of collagen fibers for successful organization.
31. Periodontal features of scurvy:
▪ Gingiva is often swollen, red and edematous.
▪ Inflammation often involves free gingiva, attached gingiva and alveolar
mucosa.
▪ Gingiva becomes brilliant red, tender and grossly swollen.
▪ Spontaneous bleeding or bleeding on gentle stimulation such that while
chewing is common.
▪ On long standing, the color may change to dark blue or purple.
▪ Ulceration may occur leading to secondary infections.
▪ Alveolar bone resorption with increased tooth mobility is seen.
32. •Ascorbic acid contributes to the formation of collagen, bone matrix
(glycosaminoglycans), and the intercellular cement substance of the
endothelial compartment in the vascular tree.
•It helps in the hydroxylation of lysine and proline which occurs in the
formation or synthesis of collagen molecule.
•It is also associated with alkaline phosphatase enzyme, the activity of
which is reduced in ascorbic acid-deficiency.
•A deficiency of ascorbic acid impairs the phagocytic activity of the
leucocytes, thereby increasing the vulnerability of dentogingival
junction.
•Ascorbic acid supplements help in the stimulation of Hexose
monophosphate shunt of neutrophils thus increasing their
chemotactic ability.
33. Vitamin B-complex
▪ The vitamin B-complex refers to all of the known essential water-soluble
vitamins except for vitamin C. These include:
• Thiamine (vitamin B1)
• Riboflavin (vitamin B2)
• Niacin (vitamin B3)
• Pantothenic acid (vitamin B5)
• Pyridoxine (vitamin B6)
• Biotin
• Folic acid and
• The cobalamins (vitamin B12).
34. Vitamin B1 (thiamin):
▪ A deficiency in thiamin intake leads to a severely reduced capacity of
cells to generate energy.
▪ The earliest symptoms of thiamin deficiency include constipation,
appetite suppression, and nausea, mental depression, peripheral
neuropathy, and fatigue.
▪ Chronic thiamin deficiency leads to more severe neurological symptoms
and to cardiovascular and musculature defects (Winston et al. 2000).
35. Vitamin B2 (riboflavin):
▪ Riboflavin deficiencies are rare in developed countries due to the
presence of adequate amounts of the vitamin in eggs, milk, meat, and
cereals (Subar et al. 1995).
▪ Riboflavin deficiency is also often seen in chronic alcoholics due to their
poor dietetic habits. Symptoms associated with riboflavin deficiency
include glossitis, seborrhea, angular stomatitis, cheilosis, and
photophobia.
Vitamin B3 (niacin):
▪ A diet deficient in niacin leads to glossitis, dermatitis, weight loss,
diarrhea, depression and dementia.
36. VitaminB7 (biotin):
▪ Biotin is found in numerous foods and is also synthesized by intestinal
bacteria, making deficiencies of the vitamin rare.
▪ Deficiencies are generally seen only after long antibiotic therapies, which
deplete the intestinal flora
Vitamin B12 (cobalamin):
▪ Vitamin B12 is synthesized exclusively by microorganisms and is found in
the liver of animals bound to protein as methycobalamin or 5'-
deoxyadenosylcobalamin.
▪ The vitamin must be hydrolyzed from protein in order to be active.
▪ Pernicious anemia is a megaloblastic anemia resulting from vitamin B12
deficiency that develops as a result of a lack of intrinsic factor in the
stomach leading to malabsorption of the vitamin.
37. Vitamin Bc (folic acid):
▪ The most pronounced effect of folate deficiency on cellular processes is
on DNA synthesis, which leads to cell cycle arrest in the S-phase of
rapidly proliferating cells, in particular hematopoietic cells, resulting in
megaloblastic anemia.
▪ The predominant causes of folate deficiency are:
▫ impaired absorption or metabolism
▫ Certain drugs such as anticonvulsants and oral contraceptives
▫ an increased demand for the vitamin
▫ Poor dietary habits
.
38. ▪ Daily folate requirement is dependent on metabolic and cell turnover
rates.
▪ Stress, such as infections increases metabolic rate and therefore
increases folate requirements.
▪ Deficiency of folate leads to impaired DNA production and asynchronism
between protein synthesis and cell division which prevent cell maturation
from reaching completion, as a consequence of which epithelial barrier
function is impaired.
▪ Folate deficiency has also been related to a decrease in host
immunocompetence .
39. ▪ Changes in female sex hormone levels, as seen during ovulation,
menstruation and pregnancy and in women taking oral contraceptives
are associated with a decreased resistance of the periodontium to local
etiologic factors, thereby resulting in increased gingival inflammation.
▪ Vogel and his associates postulated that the decreased resistance of
the gingiva to inflammatory changes associated with pregnancy and the
use of oral contraceptives may be related in part to the suboptimal levels
of folic acid in the gingiva.
▪ The results of the above study indicated that the women on oral
contraceptives develop megaloblastic changes in the sulcular epithelium,
which are reversed on folate supplementation for 60 days. This reduction
is attributable to a decrease in permeability of the sulcular epithelium,
thereby decreasing gingival inflammation
42. Minerals
Calcium • Muscle contraction
• Blood clotting •Nerve
impulse transmission
• Calcification of bone
and tooth structure
Osteoporosis
Incomplete
calcification of hard
tissues
Toxicity: not seen
Dairy products, fortified
orange juice, soy milk,
green leafy vegetables,
canned salmon and
sardine bones
Phosphorus • Required for bone and
teeth strength
• Acid-base balance
• Muscle contraction
• Poor bone
maintenance
• Incomplete
calcification of teeth
• Compromised
alveolar integrity
• Toxicity: skeletal
porosity
Dairy products, meat,
poultry, processed
foods, soft drinks, nuts,
legumes, whole grain
cereals
43. Magnesium •Bone strength and
rigidity
•Hydroxyapatite crystal
formation
•Nerve impulse •Muscle
contraction
Alveolar bone fragility
Toxicity seen in
medications containing
magnesium
Muscle weakness
Wheat bran, whole
grains, green leafy
vegetables, legumes,
nuts, chocolate
Fluoride Prevention of caries •Increased incidence of
caries
•Toxicity: tooth mottling,
enamel hypoplasia
Fluoridated water, tea,
seaweed, toothpaste
Iron Component of
hemoglobin
Carries oxygen to cells
Immune function
Cognitive development
Anemia:pallor of face,
conjunctiva, lips,
mucosa, and gingiva
Shortness of
breath,fatigue.
Decreased immunity
Toxicity: Gl upset;
pigmentation; seen in
persons with
hemochromatosis
Meat, poultry, fish,
whole grains, dried fruit,
enriched grains
44. Zinc •Required for >100
enzymes
•Normal growth and
development
•Taste and smell
sensitivity
•Sexual development
and reproduction
•Immune integrity
•Wound healing
Altered taste
Growth retardation
Decreased wound
healing
Impaired immunity
Toxicity: rare (stomach
irritation, cramps,
diarrhea, vomiting)
Seafood, meats, whole
grains, greens
Copper •Aids in iron
metabolism
•Collagen formation
Anemia
Poor growth
Low WBC
Bone demineralization
Tissue fragility
Decreased trabeculae
of alveolar bone
Toxicity: vomiting,
diarrhea
Whole grains, nuts,
dried fruits, legumes,
shell fish, organ meats
45. Calcium and periodontium
▪ Rats placed on calcium-deficient diet showed osteoporotic changes
in alveolar bone, reduction in the number and diameter of PDL fibers
and reduction in amount of secondary cementum (Fergusson and
Oliver, 1969).
▪ It also showed to stimulate osteoclastic activity (Roberts,1975).
▪ Patients with osteoporosis are at increased risk for attachment loss
(Rondoros et al 2000).
▪ Krall et al., (2001) studies suggested that low dietary intake of
calcium may result in severe progression of periodontal diseases
46. Magnesium and periodontium
▪ Widening of PDL has been observed with magnesium deficiency
(Klein et al 1935). Animal as well as clinical studies suggested that
Mg supplementation may prevent or retard periodontitis (Meyle et
al 1987).
▪ High Mg concentrations inhibit free-radical generation; activation of
neutrophils is an early effect of hypomagnesaemia (Bussiere et al
2002).
▪ Mg deficiency is also associated with low bone mass, which is
manifested in the oral cavity as loss of alveolar crestal bone height
and tooth loss, accompanied by stimulation of pro-inflammatory
cytokines (Wactawski-Wende 2001).
47. Iron and periodontium
▪ Severe iron deficiency has been related to periodontal destruction in
dogs (Hall and Robinson, 1937).
▪ Laison et al (1968) gained the impression that patients with
moderate to severe periodontitis sometimes had subnormal levels
of iron.
▪ Iron deficiency is also associated with decreased lymphocyte
proliferation, neutrophil chemotactic activity and antibody response .
48. Zinc and periodontium
•Zinc helps in stabilization of membranes, antioxidant activity,
collagen synthesis, inhibition of mast cell release of histamine.
• Zinc deficiency is associated with decreased antibody response,
phagocytic function of macrophages and B-cell and T-cell
proliferation.
•Thus supplementation of zinc may help in treatment of periodontal
diseases as an adjuvant.
49. Fluoride and periodontium
▪ Fluoride appears to reduce the destructive effects of excessive
orthodontic tooth movement in rats (Singer et al 1967).
▪ Studies suggested that the reduced severity of periodontal
diseases was either an indirect effect of the lower prevalence of
caries or a direct effect of fluoride on alveolar bone resorption.
50.
51. THERE IS CONTINOUS SYNERGY BETWEEN NUTRITION
AND INTEGRITY OF ORAL CAVITY IN HEALTH AND
DISEASE (MOYNIHAN 2005)
MALNUTRITION MAY AFFECT THE DEVELOPMENT
OF THE ORAL CAVITY AND THE PROGRESSION OF
ORAL DISEASES THROUGH ALTERED TISSUE
HOMEOSTASIS, REDUCED RESISTANCE TO
MICROBIAL BIOFILMS AND REDUCED TISSUE
REPAIR CAPACITY (LACOPINO ET AL 2006)
52. Interaction of immunity, infection, and nutritional status
▪ Nutrition is a "critical determinant of immune responses" 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 stream, lymph nodes and
specialized immune system of the gastrointestinal tract.
▪ The effects of these nutrients are dependent on several factors:
(1) The concentration of a nutrient and its interactions with other key
nutrients.
(2) The duration of the nutrient imbalance, and
(3) The age of the host. Conversely, a majority of nutrient deficiencies
will impair the immune response and predispose the individual to
infection.
53. Nutrient Function Deficiency impact or Immune response
Protein Energy intake Energy metabolism
o DNA/RNA Synthesis
↓ Salivary antimicrobial properties
↓ Immunoglobulin production
↓ Iysozymes
↑ Bacterial Adhesion
↓ Activation of lymphocytes
↓ Production of antibodies
Vitamin A Cellular differentiation and
proliferation
Integrity of the immune
System
↓ Immune cell differentiation
↓ Response to antigens
↓ Antibody production
↑ Bacterial adhesion
↓ Immunoglobulin production
↓ Production of lymphocytes
Vitamin E Antioxidant protecting lipid
membranes from oxidation
↓ Antibody synthesis
↓ Response of Lymphocytes
↓ Phagocytic function
54. Vitamin E Antioxidant protecting lipid membranes
from oxidation
↓ Antibody synthesis
↓ Response of Lymphocytes
↓ Phagocytic function
Vitamin C Antioxidant that reduces free radicals
that cause DNA damage to immune
cells
↓ Phagocytic function of neutrophils &
macrophages
↓ Antibody response
↓ Cytotoxic T-cell Activity
Riboflavin, Vitamin B6, and
panthothenic acid
Coenzymes in metabolic processes ↓ Antibody synthesis
↓ Cytotoxic T-cell activity
↓ Lymphocyte response
Folic acid and Vitamin B12 Involved in DNA / RNA synthesis ↓ Production of lymphocytes
↓ Cytotoxic T-cell activity
↓ Phagocytic function of neutrophils
Zinc Protein catabolism and synthesis
Nucleic acid synthesis
↓ Antibody response
↓ Phagocytic function of macrophages
↓ B-cell and T-cell proliferation
Iron Involved in hemoglobin, myoglobin,
cytochrome systems
↓ Lymphocyte proliferation
↓ Neutrophil cytotoxic activity
55. Effects of nutritional supplements on wound healing
▪ Alvarez & Gilbreath (1982) - demonstrated a definite involvement of
thiamine in wound repair and scar development.
▪ Aprahamian et al. (1985) - suggested that vitamin B5 induces an
accelerating effect of the normal healing process.
▪ However, megadoses of vitamin C have not been shown to have a
strong effect on the healing response in initial periodontal therapy
and, therefore, pharmacologic doses should not be recommended to
patients until further research confirms its utility. Vitamin A is
involved in collagen metabolism by affecting cell differentiation.
56. ▪ Boron, copper, manganese, silicon, and zinc are also important
participants in collagen metabolism and wound healing. Copper in
particular is an essential nutrient for the cross-linking of both collagen
and elastin.
▪ Zinc is important for its effect on protein synthesis including DNA and
RNA synthesis. Zinc concentrations increase around the wound
margin during formation of granulation tissue, scar formation, and re-
epithelization. Zinc, copper, and iron all compete for absorption so
they need to be kept in balance for optimum wound healing.
57.
58. Conclusion
In conclusion, although periodontal
disease is not a nutritional deficiency
disease per se, malnutrition is likely to
play a role in either predisposing the host
to the progression of preexisting
periodontal lesions, influence the outcome
of periodontal treatment, or both.
59. References
• Carranza’s clinical Periodontology – 11th Edition
• Textbook of biochemistry U.Satyanarayana
• Effects of specific nutrients on periodontal disease onset,
progression and treatment. J Clin Periodontol 2003; 30:579-589
• Journal of clinical Periodontology 2003; 30:579-589.
• Nutrition, infection and periodontal disease – DCNA 2003;
47(2):337-354
Editor's Notes
The World Health Organization
defines malnutrition as the cellular
imbalance between supply of nutrients
and energy and the body's demand for
them to ensure growth, maintenance,
and specific functions1