This document discusses the nutritional influence on periodontium. It begins by stating that nutritional deficiencies alone cannot cause gingivitis or periodontitis, but can affect periodontal condition and exacerbate plaque-induced inflammation. It then discusses various nutritional deficiencies and their oral manifestations, including alterations to lips, oral mucosa, gingiva and bone. Key sections explore the roles of carbohydrates, vitamins, antioxidants, and minerals on periodontal health. Specific vitamin deficiencies like Vitamins A, D, C, and B-complex are examined in depth for their periodontal effects.

1. NUTRITIONAL INFLUENCE ON
PERIODONTIUM

2. DONE BY SS YASMIN PARVIN
DEPARTMENT OF PERIODONTICS
POSTGRADUATE STUDENT
GUIDED BY
DR.J.SELVAKUMAR
PROFESSOR & HEAD OF DEPARTMENT
DEPARTMENT OF PERIODONTICS

3. INTRODUCTION :
• THE MAJORITY OF OPINION AND RESEARCH FINDINGS ON
THE EFFECTS OF NUTRITION ON ORAL AND PERIODONTAL
TISSUES POINT TO THE FOLLOWING:
1.THERE ARE NO NUTRITIONAL
DEFICIENCES THAT BY THEMSELVES CAN
CAUSE GINGIVITIS OR PERIODONTITIS:
2.THERE ARE NUTRITIONAL DEFICIENCES
THAT PRODUCE CHANGES IN THE ORAL
CAVITY.

4. • 1.THERE ARE NO NUTRITIONAL DEFICIENCES THAT BY
THEMSELVES CAN CAUSE GINGIVITIS OR
PERIODONTITIS:
• HOWEVER NUTRITIONAL DEFICIENCES CAN AFFECT THE
CONDITION OF THE PERIODONTIUM AND THERBY MAY
ACCENTUATE THE DELETERIOUS EFFECTS OF PLAQUE
INDUCED INFLAMMATION IN SUCEPTIBLE INDIVIDUALS.
• THEORECTICALLY , ONE MIGHT PRESUME THAT AN
INDIVIDUAL WITH A NUTRITIONAL DEFICIENCY IS ABLE
TO DEFEND AGAINST A BACTERIAL CHALLENGE
COMPARED WITH A NUTRITIONALLY COMPETENT
INDIVIDUAL.

5. 2.THERE ARE NUTRITIONAL DEFICIENCES THAT
PRODUCE CHANGES IN THE ORAL CAVITY.
• THESE CHANGES INCLUDE ALTERATION OF
TISSUE OF THE LIPS , ORAL MUCOSA ,GINGIVA,
GINGIVA AND BONE.
• THESE ALTERATION ARE CONSIDERED TO BE
PERIODONTAL AND ORAL MANIFESTATION OF
NUTRITIONAL DISEASE.

6. PHYSICAL NATURE OF THE DIET:
1.PHYSICAL CHARACTER OF THE DIET MAY PLAY SOME
ROLE IN THE ACCUMULATION OF PLAQUE AND
2.THE DEVELOPMENT OF GINGIVITIS.
SOFT DIETS, ALTHOUGH NUTRITIONALLY ADEQUATE,
MAY LEAD TO PLAQUE AND CALCULUS FORMATION.
3.HARD, FIBROUS FOODS PROVIDE SURFACE
CLEANSING ACTION AND STIMULATION, WHICH RESULTS
IN LESS PLAQUE AND GINGIVITIS, EVEN IF THE DIET IS
NUTRITIONALLY INADEQUATE.

7. EFFECT OF NUTRITION ON ORAL
MICROORGANISMS
• ALTHOUGH DIETARY INTAKE IS GENERALLY THOUGHT OF
IN TERMS OF SUSTAINING THE INDIVIDUAL, IT IS ALSO THE
SOURCE OF NUTRIENTS
• FOR BACTERIAL' THROUGH ITS EFFECTS ON THE ORAL
BACTERIA, THE DIET MAY INFLUENCE RELATIVE
DISTRIBUTION OF TYPES OF ORGANISMS, THEIR METABOLIC
ACTIVITY, AND THEIR PATHOGENIC POTENTIAL, WHICH IN
TURN AFFECT THE OCCURRENCE AND SEVERITY OF ORAL
DISEASE.

8. • SOURCES OF NUTRIENTS FOR THE MICROORGANISMS
CAN
BE ENDOGENOUS AND EXOGENOUS.
• AMONG THE EXOGENOUS FACTORS, THE INFLUENCE
OF
THE SUGAR CONTENT OF THE DIET HAS
BEEN EXTENSIVELY STUDIED, AND IT HAS BEEN
DEMONSTRATED
THAT THE AMOUNT AND TYPE OF CARBOHYDRATES IN
THE DIET
AND THE FREQUENCY OF INTAKE CAN INFLUENCE
BACTERIAL

9. • ATTACHMENT AND SUBSEQUENT COLONIZATION
OF
THE TOOTH SURFACE BY CERTAIN
MICROORGANISMS
ALSO MAY BE MADE POSSIBLE BY COMPONENTS
OF THE
DIET.

10. ROLE OF KEY NUTRIENTS IN
PERIODONTAL HEALTH:
• CARBOHYDRATES AND PERIODONTAL HEALTH
• VITAMINS AND PERIODONTAL HEALTH
• ANTIOXIDANTS AND PERIODONTAL HEALTH:
1.VITAMINS AS ANTIOXIDANTS A, C, E
2.LYCOPENE
3.MELATONIN
• DIETARY MINERALS AND TRACE ELEMENTS:

11. ROLE OF CARBOHYDRATE IN
PERIODONTIUM:
• SUGARS CONTRIBUTE TO DENTAL CARIES AND PERIODONTAL
DISEASE BECAUSE BACTERIA FERMENT THEM AND PRODUCE ACID,
LEADING TO THE DEMINERALIZATION OF THE TOOTH STRUCTURE.
• XYLITOL, A SUGAR ALCOHOL PRODUCED BY THE HYDROGENATION
OF XYLOSE SUGAR, IS AN ARTIFICIAL SWEETENER USED AS AN
ALTERNATIVE TO CONVENTIONAL SUGARS.
• IT MAY HAVE AN ANTIBACTERIAL EFFECT AGAINST PERIODONTAL
PATHOGENS SUCH AS PORPHYROMONAS GINGIVALIS AND
AGGREGATIBACTER ACTINOMYCETEMCOMITANS.

12. • HENCE, A REDUCTION OF SUGAR INTAKE,
COUPLED WITH SCALING, ROOT PLANING, AND
THE USE OF XYLITOL- AND MALTITOL-
CONTAINING GUMS HAVE THE POTENTIAL TO
IMPROVE THE PERIODONTAL HEALTH OF THE
GENERAL POPULATION.

13. NUTRITIONAL DEFICIENCES:
1.FAT SOLUBLE VITAMIN DEFICIENCY
2.WATER SOLUBLE VITAMIN DEFICIENCY
3.PROTEIN DEFICIENCY

14. • NUTRITIONAL DEFICIENCY OF VITAMINS
RESULTS IN ORAL MANIFESTATIONS SUCH AS
SCURVY AND RICKETS.

15. VITAMIN DEFICIENCY
• FAT SOLUBLE VITAMIN
DEFICIENCY:
1)VITAMIN A DEFICIENCY
2)VITAMIN D DEFICIENCY
3)VITAMIN E DEFICIENCY
4)VITAMIN K DEFICIENCY
• WATER SOLUBLE VITAMIN
DEFICIENCY:
1) B-COMPLEX DEFICIENCY
 THIAMIN
 RIBOFLAVIN
 NIACIN
 PYRIDOXINE B6
 BIOTIN
 FOLIC ACID
 COBALAMIN B12
1) VITAMIN C (ASCORBIC ACID )
DEFICIENCY

16. FAT-SOLUBLE VITAMIN
DEFICIENCY
• VITAMINS A, D, E AND K ARE FAT-SOLUBLE VITAMINS
REQUIRED IN THE HUMAN DIET.

17. VITAMIN A
• VITAMIN A IS A FAT-SOLUBLE VITAMIN THAT PLAYS A ROLE IN
MAINTAINING THE INTEGRITY OF EPITHELIAL CELLS .
• DIETARY SOURCES OF VITAMIN A INCLUDE EGGS, COD LIVER OIL,
CARROTS,
CAPSICUM, LIVER, SWEET POTATO, BROCCOLI, AND LEAFY
VEGETABLES.
• A HEALTHY INDIVIDUAL NEEDS APPROXIMATELY
900G/DAY.
• DEFICIENCY RESULTS IN RETINAL DISORDERS (SUCH AS
NIGHT BLINDNESS AND HYPERKEROTOSIS.
CONSIDERING THE
• ANTIOXIDANT POTENTIAL, VITAMIN A HAS BEEN USED TO
SUPPLEMENT PERIODONTAL TREATMENT

18. VITAMIN A DEFICIENCY:
• FUNCTION OF VITAMIN A – MAINTAIN THE HEALTH OF
EPITHELIAL CELLS OF THE SKIN AND MUCOUS MEMBRANE.
• DEFICIENCY RESULTS
1)DERMATOLOGIC MANIFESTATION
2)MUCOSAL MANIFESTATION
3)OCULAR MANIFESTATION
BCOZ EPITHELIAL TISSUES PROVIDE A PRIMARY BARRIER
FUNCTION TO PROTECT AGAINST INVADING
MICROORGANISM .
VITAMIN A PLAY AN IMPORTANT ROLE IN PROTECTING
AGAINST MICROBIAL INVASION BY MAINTAINING EPITHELIAL
INTEGRITY

19. • VITAMIN A DEFICIENCY RESULTS IN
HYPERKERATOSIS AND HYPERPLASIA OF THE
GINGIVA WITH A TENDENCY FOR INCREASED
PERIODONTAL POCKET FORMATION.
• HYPERPLASIA AND HYPERKERATINIZATION
OF THE GINGIVAL EPITHELIUM WITH
PROLIFERATION OF
THE JUNCTIONAL EPITHELIUM AND RETARDATION
OF GINGIVAL WOUND HEALING.

20. VITAMIN D DEFICIENCY/
CALCIFEROL:
• ESSENTIAL FOR ABSORPTION OF CALCIUM FROM THE GIT
AND MAINTANENCE OF THE CALCIUM- PHOSPHORUS
BALANCE.
• DEFICIENCY IN VITAMIN D AND IMBALANCE IN CALCIUM –
PHOSPHOROUS INTAKE RESULTS IN RICKETS IN YOUNG
CHILDREN AND OSTEOMALACIA IN ADULTS.
• RESULTS IN OSTEOPOROSIS OF ALVEOLAR BONE OF
PERIODONTAL TISSUE.
• OSTEOID THAT FORM AT NORMAL RATE BUT REMAINS
UNCALCIFIED.
• FAILURE OF OSTEOID TO RESORB , WHICH LEADS TO ITS

21. • VITAMIN D IS REQUIRED FOR A NUMBER OF ESSENTIAL
FUNCTIONS
IN THE BODY. IT ENHANCES THE ABSORPTION OF MINERALS
INCLUDING
CALCIUM, MAGNESIUM, IRON, PHOSPHATE, AND ZINC IN THE
INTESTINE.
• IN HUMANS, THERE ARE TWO IMPORTANT GROUPS OF
VITAMIN D, VITAMINS D2 (CHOLECALCIFEROL) AND D3
(ERGOCALCIFEROL).
• CLINICAL STUDIES HAVE SUGGESTED THAT A
DEFICIENCY OF DIETARY VITAMIN D LEADS TO PERIODONTAL
INFLAMMATION AND A DELAY IN POST-SURGICAL PERIODONTAL

22. • REDUCTION IN THE WIDTH OF THE PERIODONTAL LIGAMENT
SPACE; A NORMAL RATE OF CEMENTUM FORMATION, BUT
DEFECTIVE CALCIFICATION AND SOME CEMENTUM RESORPTION;
AND DISTORTION OF THE GROWTH PATTERN OF ALVEOLAR
BONE.
• THERE IS RAPID, GENERALIZED,
SEVERE OSTEOCLASTIC RESORPTION OF ALVEOLAR BONE,
PROLIFERATION
OF FIBROBLASTS THAT REPLACE BONE AND MARROW, AND
NEW BONE FORMATION AROUND THE REMNANTS OF UN
RESORBED
BONY TRABECULAE

23. • RADIOGRAPHICALLY, THERE IS GENERALIZED PARTIAL TO
COMPLETE
DISAPPEARANCE OF THE LAMINA DURA AND REDUCED
DENSITY OF
THE SUPPORTING BONE, LOSS OF TRABECULAE,
INCREASED RADIOLUCENCE OF THE TRABECULAR
INTERSTICES,
AND INCREASED PROMINENCE OF THE REMAINING
TRABECULAE.

24. VITAMIN E DEFICIENCY:
• ANTIOXIDANT TO LIMIT FREE –RADICAL REACTION AND
TO PROTECT CELLS FROM LIPID PEROXIDATION
• CELL MEMBRANES WHICH ARE HIGH IN
POLYUNSATURATED LIPIDS ARE MAJOR SITE OF
DAMAGE IN VITAMIN E DEFICIENCY.
• SYSTEMIC VITAMIN E APPEARS TO ACCELETATE
GINGIVAL WOUND HEALING IN THE RATS.

25. • VITAMIN E (TOCOPHEROL) IS A FAT-SOLUBLE VITAMIN THAT IS
CONSIDERED ONE OF THE KEY EXTRACELLULAR
ANTIOXIDANTS.
• DIETS RICH IN VITAMIN E INCLUDE POULTRY, MEAT, FISH,
NUTS, SEEDS, AND CEREALS .
• VITAMIN E STABILIZES THE MEMBRANE STRUCTURE BY
TERMINATING THE FREE RADICAL REACTION .
• THERE WERE NO REMARKABLE DIFFERENCES IN THE
PLASMA LEVEL OF VITAMIN E IN HEALTHY INDIVIDUALS
COMPARED TO PATIENTS WITH PERIODONTITIS
• IN CONTRAST, A FEW STUDIES REPORTED FAVORABLE
EFFECTS OF
VITAMIN E IN MAINTAINING PERIODONTAL HEALTH AND
CONTROLLING

26. • IN ADDITION, A REDUCTION OF VITAMIN E WAS OBSERVED IN
PATIENTS WITH PERIODONTAL DISEASES COMPARED TO
HEALTHY
INDIVIDUALS. THE LEVEL OF VITAMIN E IN THE ALVEOLAR
FLUID OF SMOKERS IS REDUCED, CORRESPONDING TO
INCREASED
PRODUCTION OF OXIDANTS DURING SMOKING. THE
MECHANISM
OF ACTION OF VITAMIN E FOR PERIODONTAL HEALTH IS NOT
VERY WELL
UNDERSTOOD AND NEEDS FURTHER RESEARCH

27. VITAMIN K
• VITAMIN K IS A GROUP OF VITAMINS REQUIRED FOR THE SYNTHESIS
OF PROTEINS THAT ARE PRECURSORS OR PREREQUISITES OF THE
FORMATION OF BLOOD COAGULATION FACTORS SUCH AS
PROTHROMBIN AND FACTORS VII, IX, AND X .
• IN ADDITION, RESEARCH HAS INDICATED THAT VITAMIN K ALSO
PLAYS A ROLE IN THE FORMATION OF PROTEINS REQUIRED FOR
BONE METABOLISM SUCH AS OSTEOCALCIN AND PERIOSTIN.
• A NUMBER OF FOODS SUCH AS KALE, SPINACH, COLLARDS, AND
MUSTARD ARE A SOURCE OF VITAMIN K1. HOWEVER, VITAMIN K2
DEFICIENCY IS RARE OWING TO THE FACT THAT ANAEROBIC
BACTERIA PRESENT IN THE GUT CAN CONVERT VITAMIN K1 TO K2.
• NEVERTHELESS, INTAKE OF ANTIBIOTICS MAY DISRUPT THE
BALANCE OF INTESTINAL BACTERIA, LEADING TO A DEFICIENCYOF
VITAMIN K

28. • HENCE, IF ANTIBIOTICS ARE TO BE MADE PART OF
PERIODONTAL THERAPY FOR A LONG PERIOD OF TIME,
COAGULOPATHIES MIGHT BE OBSERVED. VITAMIN K IS AN
IMPORTANT PHARMACOLOGICAL AGENT USED TO
REVERSE THE ANTICOAGULANT EFFECTS OF WARFARIN
AND ROUTINELY ADMINISTERED FOR PATIENTS
UNDERGOING HEMODIALYSIS .
• HENCE, IF PERIODONTAL THERAPY IS TO BE
ADMINISTERED TO PATIENTS WITH KIDNEY FAILURE,
VITAMIN K CAN BE USED TO TREAT ANY BLEEDING
INCIDENTS.

29. • THE ROUTINE DIET PROVIDES ENOUGH VITAMIN K FOR A
HEALTHY INDIVIDUAL, HENCE THE DEFICIENCY OF
VITAMIN IS VERY RARE.
• HOWEVER, A PATIENT WITH DIGESTIVE DISORDER OR
WHO HAS BEEN USING ANTIBIOTICS FOR A LONG PERIOD
OF TIME MUST BE INVESTIGATED FOR VITAMIN K
DEFICIENCY .
• ALTHOUGH VITAMIN K DEFICIENCY MAY LEAD TO
GINGIVAL BLEEDING, A RECENT STUDY BY ARAL ET AL.
HAS FOUND THAT VITAMIN K SUPPLEMENTATION WAS
NOT ABLE TO REDUCE PRO-INFLAMMATORY FACTORS IN
THE PERIODONTIUM.

30. WATER SOLUBLE VITAMIN
DEFICIENCY: B COMPLEX &
VITAMIN C
• VITAMINS B AND C ARE WATER-SOLUBLE VITAMINS
REQUIRED IN
THE HUMAN DIET.
 THE FUNCTION OF THESE VITAMINS AND THE
CLINICAL MANIFESTATIONS OF THEIR DEFICIENCY ARE
DESCRIBED
IN THIS SECTION.

31. • THE VITAMIN B COMPLEX FAMILY CONSISTS OF VITAMINS B1
(THIAMINE), B2 (RIBOFLAVIN), B3 (NIACIN),B5 (PANTOTHENIC
ACID), B6 (PYRIDOXINE, PYRIDOXAL, PYRIDOXAMINE) B7
(BIOTIN),
B9 (FOLIC ACID), AND B12(COBALAMINS). B VITAMINS PLAY A
VITAL
ROLE IN CELL METABOLISM, REPAIR, AND PROLIFERATION.
DEFICIENCY
OF B VITAMINS RESULTS IN A NUMBER OF DISEASES AND
SYMPTOMS

32. VITAMIN B COMPLEX
DEFICIENCY:
• THE VITAMIN B COMPLEX INCLUDES
1.THIAMIN
2. RIBOFLAVIN
3. NIACIN
4.PYRIDOXINE (B6)
5. BIOTIN,
FOLIC ACID, AND COBALAMIN (B IZ ).

33. • ORAL DISEASE IS RARELY DUE TO
A DEFICIENCY IN JUST ONE COMPONENT OF THE B-
COMPLEX
GROUP, THE DEFICIENCY IS GENERALLY MULTIPLE.
• ORAL CHANGES COMMON TO B-COMPLEX DEFICIENCIES
ARE
• 1.GINGIVITIS
• 2.GLOSSITIS
• 3.GLOSSODYNIA,
• 4.ANGULAR CHEILITIS, AND
• 5. INFLAMMATION OF THE ENTIRE ORAL MUCOSA.

34. • THE GINGIVITIS IN
VITAMIN B DEFICIENCIES IS NONSPECIFIC, AS IT IS CAUSED BY
BACTERIAL PLAQUE RATHER THAN BY THE DEFICIENCY, BUT
IT IS
SUBJECT TO THE MODIFYING EFFECT OF THE LATTER.
• 1.ORAL MANIFESTATIONS OF VITAMIN B-COMPLEX
DEFICIENCY IN EXPERIMENTAL ANIMALS INCLUDE
• 2. BLACK TONGUE
• 3. GINGIVAL INFLAMMATION WITH DESTRUCTION OF THE
GINGIVA,
• PERIODONTAL LIGAMENT, AND
• 4.ALVEOLAR BONE.

35. THIAMIN DEFICIENCY
• THE HUMAN MANIFESTATIONS OF THIAMIN
DEFICIENCY,
CALLED BERIBERI. FRANK BERIBERI IS RARE.
• CHARACTERIZED BY
• 1. PARALYSIS;
• 2.CARDIOVASCULAR
SYMPTOMS,
3. INCLUDING EDEMA; AND
4. LOSS OF APPETITE.

36. • ORAL DISTURBANCES
THAT HAVE BEEN ATTRIBUTED TO THIAMIN
DEFICIENCY
INCLUDE
• 1. HYPERSENSITIVITY OF THE ORAL MUCOSA;
• 2. MINUTE VESICLES (SIMULATING HERPES) ON THE
BUCCAL MUCOSA
• 3.UNDER THE TONGUE, OR ON
• 4. THE PALATE; AND
• 5.EROSION OF THE ORAL
MUCOSA.

37. RIBOFLAVIN DEFICIENCY:
• THE SYMPTOMS OF RIBOFLAVIN DEFICIENCY
(ARIBOFLAVINOSIS)
INCLUDE GLOSSITIS, ANGULAR CHEILITIS, SEBORRHEIC
DERMATITIS,
AND A SUPERFICIAL VASCULARIZING KERATITIS.
• THE GLOSSITIS IS CHARACTERIZED BY A MAGENTA
DISCOLORATION
• AND ATROPHY OF THE PAPILLAE.
• IN MILD TO MODERATE CASES,THE DORSUM EXHIBITS A
PATCHY
• ATROPHY OF THE LINGUAL PAPILLAE AND ENGORGED
FUNGIFORM
• PAPILLAE, WHICH PROJECT AS PEBBLE-LIKE ELEVATIONS.

38. • 1.ANGULAR CHEILITIS BEGINS AS AN INFLAMMATION OF
THE
COMMISSURE OF THE LIPS, FOLLOWED BY EROSION,
ULCERATION,
AND FISSURING.
• 2.RIBOFLAVIN DEFICIENCY IS NOT THE ONLY CAUSE OF
ANGULAR CHEILITIS.
• 3.LOSS OF VERTICAL DIMENSION, TOGETHER
WITH DROOLING OF SALIVA INTO THE ANGLES OF THE LIPS,
MAY
PRODUCE A CONDITION SIMILAR TO ANGULAR CHEILITIS.
• 4.CANDIDIASIS MAY DEVELOP IN THE COMMISSURES OF

39. CHANGES OBSERVED IN RIBOFLAVIN-
DEFICIENCY INCLUDE
1.SEVERE LESIONS OF THE GINGIVAE;
2. PERIODONTAL TISSUES;
3. AND ORAL MUCOSA, INCLUDING NOMA.

40. NIACIN DEFICIENCY
• NIACIN DEFICIENCY RESULTS IN
1. PELLAGRA, WHICH IS CHARACTERIZED
BY DERMATITIS;
2.GASTROINTESTINAL DISTURBANCES;
3.NEUROLOGIC AND MENTAL DISTURBANCES
(DERMATITIS, DIARRHEA,
AND DEMENTIA
4.GLOSSITIS

41. 5. GINGIVITIS; AND
6. GENERALIZED STOMATITIS.
7.GLOSSITIS AND STOMATITIS MAY BE THE EARLIEST
CLINICAL
SIGNS OF NIACIN DEFICIENCY.
8.THE GINGIVA MAY BE INVOLVED IN ANIACINOSIS WITH OR
WITHOUT TONGUE CHANGES.

42. • ORAL MANIFESTATIONS OF VITAMIN NIACIN
DEFICIENCY INCLUDE
1.BLACK TONGUE
2. GINGIVAL INFLAMMATION WITH DESTRUCTION OF THE
GINGIVA,
3.PERIODONTAL LIGAMENT,
4.ALVEOLAR BONE.
5.NECROSIS OF THE GINGIVA AND OTHER ORAL TISSUES, AS
WELL AS
6.LEUKOPENIA, ARE TERMINAL FEATURES OF NIACIN
DEFICIENCY IN
EXPERIMENTAL ANIMALS.

43. FOLIC ACID DEFICIENCY
• FOLIC ACID DEFICIENCY RESULTS IN
1. MACROCYTIC ANEMIA WITH MEGALOBLASTIC ERYTHROPOIESIS,
ACCOMPANIED BY ORAL CHANGES,
2. GASTROINTESTINAL LESIONS,
3. DIARRHEA, AND
4. INTESTINAL MALABSORPTION.
• FOLIC ACID-DEFICIENT ANIMALS DEMONSTRATE
1.NECROSIS OF THE GINGIVA,
2. PERIODONTAL LIGAMENT, AND
3 .ALVEOLAR BONE WITHOUT INFLAMMATION.
• THE ABSENCE OF INFLAMMATION IS THE RESULT OF DEFICIENCY-
INDUCED GRANULOCYTOPENIA.

44. • IN HUMANS WITH SPRUE AND OTHER FOLIC ACID
DEFICIENCY
STATES, GENERALIZED STOMATITIS OCCURS, WHICH MAY
BE ACCOMPANIED BY ULCERATED GLOSSITIS AND
CHEILITIS.
• ULCERATIVE STOMATITIS IS AN EARLY INDICATION OF
THE TOXIC
EFFECT OF FOLIC ACID ANTAGONISTS USED IN THE
TREATMENT OF
LEUKEMIA.
• A SIGNIFICANT REDUCTION OF GINGIVAL INFLAMMATION
HAS BEEN
REPORTED AFTER SYSTEMIC OR LOCAL USE OF FOLIC
ACID, WHEN

45. • THIS REDUCTION OCCURRED WITH NO CHANGE
IN PLAQUE ACCUMULATION.
• GINGIVAL CHANGES ASSOCIATED WITH PREGNANCY
AND ORAL CONTRACEPTIVES MAY BE PARTLY RELATED TO
SUBOPTIMAL LEVELS OF FOLIC ACID IN THE GINGIVA.
• IN A CLINICAL STUDY OF PREGNANT WOMEN, A REDUCTION IN
GINGIVAL INFLAMMATION OCCURRED WITH THE USE OF
TOPICAL FOLATE
MOUTH RINSES; NO CHANGE WAS FOUND WITH SYSTEMIC
FOLIC ACID.

46. • A RELATIONSHIP HAS ALSO BEEN ASSUMED
BETWEEN
PHENYTOIN-INDUCED GINGIVAL OVERGROWTH
AND FOLIC ACID,
BASED ON THE INTERFERENCE OF FOLIC ACID
ABSORPTION AND
UTILIZATION OF PHENYTOIN.

47. VITAMIN C ( ASCORBIC ACID )
DEFICIENCY
• SEVERE VITAMIN C DEFICIENCY IN HUMANS RESULTS IN SCURVY
, A DISEASE CHARACTERIZED BY HEMORRHAGIC DIATHESIS AND
RETARDATION OF WOUND HEALING.
• VITAMIN C IS REQUIRED IN THE HUMAN DIET. VITAMIN C IS
ABUNDANT IN FRUITS AND VEGETABLES.
• SCURVY IS UNCOMMON IN COUNTRIES THAT HAVE ADEQUATE
FOODSUPPLIES, BUT IT MAY APPEAR IN INFANTS IN THEIR FIRST YEAR
OF
LIFE IF FORMULAS ARE NOT FORTIFIED WITH VITAMINS AND IN THE
VERY OLD, ESPECIALLY THOSE LIVING ALONE AND ON RESTRICTED
DIETS.

48. • VITAMIN C (ASCORBIC ACID) IS PRIMARILY REQUIRED FOR
THE
SYNTHESIS OF COLLAGEN AND IT ALSO PREVENTS OXIDATIVE
DAMAGE
BY ACTING AS A ROS SCAVENGER. SCURVY, FIRST IDENTIFIED
BY
SIR THOMAS BARLOW IN 1883, IS THE NAME GIVEN TO THE
DISEASE
CAUSED BY THE DEFICIENCY OF VITAMIN C.

49. • ALCOHOLISM ALSO MAY PREDISPOSE AN INDIVIDUAL TO
SCURVY.
• SCURVY CLINICAL MANIFESTATIONS OF SCURVY INCLUDE
1.HEMORRHAGIC LESIONS INTO THE MUSCLES OF THE
EXTREMITIES, THE
JOINTS, AND SOMETIMES THE NAIL BEDS;
2. PETECHIAL HEMORRHAGES, OFTEN AROUND HAIR
FOLLICLES;
3.INCREASED SUSCEPTIBILITY TO INFECTIONS; AND
4. IMPAIRED WOUND HEALING.
5.BLEEDING, SWOLLEN GINGIVA AND LOOSENED TEETH ARE
ALSO
COMMON FEATURES OF SCURVY.

50. • VITAMIN C DEFICIENCY (SCURVY) RESULTS IN
• 1. DEFECTIVE FORMATION AND
• 2.MAINTENANCE OF COLLAGEN,
• 3. RETARDATION OR CESSATION OF OSTEOID FORMATION,
AND
• 4.IMPAIRED OSTEOBLASTIC FUNCTION.
• VITAMIN C DEFICIENCY IS ALSO CHARACTERIZED
1.INCREASED CAPILLARY PERMEABILITY,
2. SUSCEPTIBILITY TO TRAUMATIC HEMORRHAGES,
3. HYPOREACTIVITY OF THE CONTRACTILE ELEMENTS OF
THE PERIPHERAL BLOOD VESSELS, AND
4.SLUGGISHNESS OF BLOOD FLOW.

51. POSSIBLE ETIOLOGIC
RELATIONSHIPS BETWEEN
ASCORBIC ACID AND PERIODONTAL
DISEASE:
IT HAS BEEN SUGGESTED THAT ASCORBIC ACID MAY PLAY A ROLE
IN
PERIODONTAL DISEASE BY ONE OR MORE OF THE FOLLOWING
MECHANISMS.
• 1. LOW LEVELS OFASCORBIC ACID INFLUENCE THE METABOLISM OF
COLLAGEN WITHIN THE PERIODONTIUM, THEREBY AFFECTING THE
ABILITY O F THE TISSUE TO REGENERATE AND REPAIR ITSELF. NO
EXPERIMENTAL EVIDENCE SUPPORTS THIS VIEW OF THE ROLE OF
ASCORBIC ACID; FURTHERMORE, IT HAS BEEN SHOWN THAT
COLLAGEN
FIBERS IN THE PERIODONTAL LIGAMENT OF SCORBUTIC MONKEYS
ARE

52. • 2. ASCORBIC ACID DEFICIENCY INTERFERES WITH BONE
FORMATION, LEADING TO LOSS OFPERIODONTAL BONE.
CHANGES
THAT DO OCCUR IN ALVEOLAR BONE AND OTHER BONES AS A
RESULT OF
FAILURE OF THE OSTEOBLASTS TO FORM OSTEOID TAKE
PLACE VERY
LATE IN THE DEFICIENCY STATE. 7 2 OSTEOPOROSIS OF
ALVEOLAR
BONE IN SCORBUTIC MONKEYS OCCURS AS A RESULTOF
INCREASED
OSTEOCLASTIC RESORPTION AND IS NOT ASSOCIATED

53. • 3. 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 OPTIMAL LEVELS OF THIS VITAMIN,
THEREFORE, WOULD THE EPITHELIUM'S BARRIER
FUNCTION TO
BACTERIAL PRODUCTS.

54. • 4. INCREASING LEVELS OF ASCORBIC ACID ENHANCE
BOTH THE
CHEMOTACTIC AND MIGRATORY ACTION OFLEUKOCYTES
WITHOUT
INFLUENCING THEIR PHAGOCYTIC ACTIVITY.MEGADOSES
OF
VITAMIN C SEEM TO IMPAIR THE BACTERICIDAL ACTIVITY
OF
LEUKOCYTES.
THE SIGNIFICANCE OF THESE FINDINGS FOR THE
PATHOGENESIS AND TREATMENT OF PERIODONTAL
DISEASES IS
NOT UNDERSTOOD.

55. • S. AN OPTIMAL LEVEL OFASCORBIC ACID IS
APPARENTLY
REQUIRED TO MAINTAIN THE INTEGRITY OFTHE
PERIODONTAL
MICROVASCULATURE, AS WELL AS THE VASCULAR
RESPONSE TO
BACTERIAL IRRITATION AND WOUND HEALING.

56. • 6. DEPLETION OF VITAMIN C MAY INTERFERE
WITH THE
ECOLOGIC EQUILIBRIUM OF BACTERIA IN
PLAQUE AND THUS INCREASE ITS
PATHOGENICITY. HOWEVER, THERE IS NO
EVIDENCE THAT DEMONSTRATES THIS EFFECT.

57. EPIDEMIOLOGIC STUDIES
• SEVERAL STUDIES IN LARGE POPULATIONS HAVE
ANALYZED THE
RELATIONSHIP BETWEEN GINGIVAL OR PERIODONTAL
STATUS AND
ASCORBIC ACID LEVELS.
• THESE STUDIES USED DIFFERENT METHODS FOR THE
BIOCHEMICAL ANALYSIS OF ASCORBIC ACID AND VARIOUS
INDICES FOR
THE ASSESSMENT OF PERIODONTAL CHANGES; THEY WERE
MADE IN
PERSONS OF DIFFERENT SOCIOECONOMIC STATUS,

58. • ALL THE EPIDEMIOLOGIC SURVEYS
FAILED TO ESTABLISH A CAUSAL RELATIONSHIP BETWEEN
THE LEVELS
OF VITAMIN C AND THE PREVALENCE OR SEVERITY OF
PERIODONTAL
DISEASE.
• MEGADOSES OF ASCORBIC ACID HAVE ALSO BEEN
FOUND TO BE
UNRELATED TO BETTER PERIODONTAL HEALTH .

59. GINGIVITIS:
• THE LEGENDARY ASSOCIATION OF SEVERE GINGIVAL
DISEASE WITH SCURVY LED TO THE PRESUMPTION THAT
VITAMIN
C DEFICIENCY IS AN ETIOLOGIC FACTOR IN GINGIVITIS,
WHICH IS COMMON AT ALL AGES.
• GINGIVITIS WITH ENLARGED, HEMORRHAGIC, BLUISH-RED
GINGIVA
IS DESCRIBED AS ONE OF THE CLASSIC SIGNS OF VITAMIN C
DEFICIENCY, BUT GINGIVITIS IS NOT CAUSED BY VITAMIN C
DEFICIENCY PER SE.

60. • VITAMIN C- DEFICIENT PATIENTS DO NOT NECESSARILY HAVE
GINGIVITIS.
• ACUTE VITAMIN C DEFICIENCY DOES
NOT CAUSE OR INCREASE THE INCIDENCE OF GINGIVAL
INFLAMMATION,
BUT IT DOES INCREASE ITS SEVERITY.
• GINGIVITIS IN VITAMIN C-DEFICIENT PATIENTS IS CAUSED BY
BACTERIAL PLAQUE.
• VITAMIN C DEFICIENCY MAY AGGRAVATE THE GINGIVAL
RESPONSE TO PLAQUE AND WORSEN THE EDEMA,
ENLARGEMENT,
AND BLEEDING.

61. • ALTHOUGH CORRECTING THE DEFICIENCY MAY
REDUCE THE SEVERITY OF THE DISORDER,
GINGIVITIS
WILL REMAIN AS LONG AS BACTERIAL FACTORS
ARE PRESENT

62. PERIODONTITIS:
• ACUTE VITAMIN C DEFICIENCY RESULTS IN
1. EDEMA
AND HEMORRHAGE IN THE PERIODONTAL LIGAMENT,
2. OSTEOPOROSIS OF THE ALVEOLAR BONE, AND
3. TOOTH MOBILITY;
4. HEMORRHAGE,
EDEMA, AND
5. DEGENERATION OF COLLAGEN FIBERS OCCUR
IN THE GINGIVA.
6.VITAMIN C DEFICIENCY ALSO RETARDS GINGIVAL
HEALING.

63. PERIODONTITIS:
• THE PERIODONTAL FIBERS THAT ARE LEAST AFFECTED
BY
VITAMIN C DEFICIENCY ARE THOSE JUST BELOW THE
JUNCTIONAL
EPITHELIUM AND ABOVE THE ALVEOLAR CREST, WHICH
EXPLAINS
THE INFREQUENT APICAL DOWN GROWTH OF THE
EPITHELIUM.
• VITAMIN C DEFICIENCY DOES NOT CAUSE PERIODONTAL
POCKETS;
LOCAL BACTERIAL FACTORS ARE REQUIRED FOR POCKET
FORMATION TO OCCUR.

64. • THE EXAGGERATED DESTRUCTION RESULTS
PARTLY FROM AN INABILITY TO MARSHAL A
DEFENSIVE DELIMITING CONNECTIVE TISSUE
BARRIER REACTION TO THE INFLAMMATION AND
PARTLY FROM DESTRUCTIVE TENDENCIES
CAUSED BY THE DEFICIENCYITSELF,INCLUDING
INHIBITION OF FIBROBLAST FORMATION AND
DIFFERENTIATION TO OSTEOBLASTS, AS WELL AS
IMPAIRED FORMATION OF COLLAGEN AND
MUCOPOLYSACCHARIDE GROUND SUBSTANCE

65. • IN A RETROSPECTIVE ANALYSIS OF 12,419 ADULTS STUDIED IN
THE THIRD NATIONAL HEALTH AND NUTRITION EXAMINATION
SURVEY (NHANES III), NISHIDA ET AL FOUND THAT THERE WAS
A WEAK BUT STATISTICALLY SIGNIFICANT DOSE-RESPONSE
RELATIONSHIP
BETWEEN THE LEVELS OF DIETARY VITAMIN C INTAKE
AND PERIODONTAL DISEASE IN CURRENT AND FORMER
SMOKERS
AS MEASURED BY CLINICAL ATTACHMENT.
• THIS SUGGESTS THAT VITAMIN C DEFICIENCY HAS ITS
GREATEST
IMPACT ON PERIODONTAL DISEASE WHEN PREEXISTING DISEASE
AND

66. • IN SUMMARY, ANALYSIS OF THE LITERATURE INDICATES
THAT
THE MICROSCOPIC SIGNS OF VITAMIN C DEFICIENCY ARE
QUITE
DIFFERENT FROM THOSE THAT OCCUR IN PLAQUE-
INDUCED
PERIODONTAL DISEASE IN HUMANS.
• PATIENTS WITH ACUTE OR CHRONIC VITAMIN C-
DEFICIENT
STATES AND NO PLAQUE ACCUMULATION SHOW MINIMAL,
IF
ANY CHANGES IN THEIR GINGIVAL HEALTH STATUS.

67. ANTIOXIDANTS AND
PERIODONTAL HEALTH:
• THE ORAL CAVITY, LIKE ANY OTHER TISSUE, UNDERGOES
INFLAMMATION AND INJURY DUE TO DISEASE AND TRAUMA.
• THE INFLAMMATORY PROCESSES INVOLVE THE
PRODUCTION OF ROS BY IMMUNE CELLS WHILE
STIMULATED BY PATHOGENS. ROS AND HIGHLY REACTIVE
FREE RADICALS (MOLECULES CONTAINING UNPAIRED
ELECTRONS) ARE CAPABLE OF INFLICTING CELLULAR AND
TISSUE DAMAGE BY ALTERING THE CHEMICAL STRUCTURE
OF MOLECULES.
• THEY PARTICULARLY DAMAGE LIPIDS BY INITIATING A CHAIN
OF LIPID PEROXIDATION

69. • FIGURE 2. PERIODONTAL DISEASE IS A COMPLEX PROCESS OF
INFECTIVE AND INFLAMMATORY PROCESSES LEADING TO
PRODUCTION
OF REACTIVE OXIDATIVE SPECIES (ROS), WHICH IN TURN WORSEN
PERIODONTITIS. ANTIOXIDANTS MAY IMPROVE PERIODONTAL
HEALTH
AND OUTCOMES OF PERIODONTAL THERAPY BY REDUCING THE
OXIDATIVE STRESS VIA SCAVENGING RO

70. • NORMALLY, AEROBIC RESPIRATION LEADS TO
THE PRODUCTION OF ROS. HOWEVER, THE
ANTIOXIDANT DEFENSE ENZYMES REDUCE THE
ROS TO MINIMIZE CELLULAR DAMAGE.
• ON THE OTHER HAND, IF THERE IS EXCESSIVE
PRODUCTION OF ROS DUE TO INFLAMMATION
OR TISSUE DAMAGE, THE ANTIOXIDANT SYSTEM
IS INSUFFICIENT TO MINIMIZE OXIDATIVE
DAMAGE.
• WHEN THIS BALANCE OF ROS PRODUCTION
AND ANTIOXIDANT ENZYMES (E.G.,
GLUTATHIONE) IS DISRUPTED, A STATE OF
OXIDATIVE STRESS OCCURS.

71. • THE PERIODONTIUM CAN ALSO ENTER A STATE OF
OXIDATIVE STRESS DUE TO THE ONSET OF
INFLAMMATION CAUSED BY DISEASE AND/OR TRAUMA.
• THE ASSOCIATION BETWEEN OXIDATIVE STRESS,
INFLAMMATION, AND INFLAMMATORY GROWTH FACTOR
IS SHOWN IN FIGURE 2. ANTIOXIDANTS MAY HELP IN
REDUCING THE SEVERITY OF DISEASE BY SCAVENGING
ROS
• . A NUMBER OF DIETARY COMPONENTS THAT CAN
FUNCTION AS ANTIOXIDANTS HAVE SHOWN POTENTIAL
FOR IMPROVING PERIODONTAL HEALTH AND HEALING.

72. VITAMINS AS ANTIOXIDANTS
• APART FROM PLAYING A VITAL ROLE IN CELL
METABOLISM, VITAMINS HAVE POTENT ANTIOXIDANT
PROPERTIES.
• VITAMINS A, C, AND E HAVE ALL BEEN OBSERVED TO
MODULATE THE ANTI‐OXIDANT DEFENSE SYSTEM.
• DIETARY VITAMINS C AND E HAVE BEEN STUDIED FOR
THEIR POTENTIAL ROLE IN REDUCING OXIDATIVE STRESS
IN THE PERIODONTIUM.
• SUPPLEMENTATION WITH VITAMIN C IN PATIENTS
UNDERGOING NON‐SURGICAL PERIODONTAL THERAPY
INCREASED THE TOTAL ANTIOXIDANT CAPACITY (TAOC);

73. • INCREASED INTAKE OF FOODS HIGH IN
VITAMINS A, C, AND E HAS BEEN OBSERVED TO
DECREASE THE SEVERITY OF PERIODONTITIS IN
NON‐SMOKERS;
• SIMILARLY, SUPPLEMENTATION WITH VITAMIN E
HAS BEEN OBSERVED TO SIMULTANEOUSLY
REDUCE LEVELS OF SERUM SUPEROXIDE
DISMUTASE AND IMPROVE THE OUTCOMES OF
SCALING AND ROOT‐PLANING .
• INDEED, MORE LONG‐TERM, WELL‐DESIGNED
STUDIES ARE REQUIRED TO ASCERTAIN THE
ANTIOXIDANT EFFECT OF VITAMIN
SUPPLEMENTATION ON PERIODONTAL AND
PERI‐IMPLANT HEALING.

74. LYCOPENE
• LYCOPENE IS A RED PIGMENT PRESENT IN VEGETABLES
SUCH AS TOMATOES, CARROTS, AND WATERMELONS.
• LYCOPENE MAY PREVENT CANCER AND CARDIAC
DISEASES DUE TO ITS ANTIOXIDANT EFFECTS .
• SIMILARLY, IN SOME STUDIES LYCOPENE HAS BEEN
INVESTIGATED AS AN ADJUNCT TO NON‐SURGICAL
PERIODONTAL THERAPY.
• A STUDY BY CHANDRA ET AL. SUGGESTED THAT
LYCOPENE SUPPLEMENTATION MAY ENHANCE THE
IMPROVEMENT OF PERIODONTAL HEALTH .

75. • SIMILARLY, LATER STUDIES HAVE ALSO FOUND
A POSSIBLE THERAPEUTIC ROLE OF LYCOPENE
IN THE MANAGEMENT OF PERIODONTITIS .
• TO DATE, THE EXACT MECHANISM OF ACTION
OF LYCOPENE IN THE PERIODONTIUM HAS NOT
BEEN ESTABLISHED.
• INDEED, THE ANTI OXIDATIVE EFFECT OF
LYCOPENE ON THE PERIODONTIUM WARRANTS
MORE RESEARCH BEFORE IT MAY BE
ADVOCATED AS A DIETARY SUPPLEMENT AS AN
ADJUNCT TO SURGICAL AND NON‐SURGICAL
PERIODONTAL THERAPY.

76. MELATONIN:
• MELATONIN IS A POTENT ANTIOXIDANT SECRETED BY
VARIOUS ORGANS OF THE HUMAN BODY.
• ADDITIONALLY, PLANTS AND CEREALS ARE SOURCES OF
MELATONIN. ALTHOUGH MELATONIN IS NOT CLASSIFIED
AS A MAJOR NUTRIENT, IT HAS BEEN SUGGESTED THAT,
IN SUPPLEMENT FORM, THE ANTI OXIDATIVE PROPERTIES
OF MELATONIN ARE MORE POTENT THAN THOSE OF
VITAMIN E .
• MORE RECENTLY, RESEARCH HAS FOCUSED ON THE
POSSIBLE THERAPEUTIC POTENTIAL OF MELATONIN
SUPPLEMENTATION IN THE ORAL CAVITY AND,
PARTICULARLY, ON THE PERIODONTIUM.

77. • TOPICAL FORMS OF MELATONIN MAY BE USED
AS AN ADJUNCT TO SURGICAL AND NON-
SURGICAL PERIODONTAL THERAPY.
• INDEED, STUDIES CONDUCTED ON ANIMALS
HAVE SHOWN THAT MELATONIN REDUCES BONE
RESORPTION CAUSED BY INDUCED
PERIODONTITIS .

78. • APART FROM THE THERAPEUTIC EFFECT OF TOPICAL
MELATONIN SUPPLEMENTATION ON PERIODONTAL
INFLAMMATION, RESEARCH HAS ALSO FOCUSED ON ITS USE
AS AN OSSEO-CONDUCTIVE AGENT AROUND DENTAL
IMPLANTS .
• MELATONIN ACTS AS AN ROS SCAVENGER AT THE SITE OF
IMPLANT PLACEMENT TO REDUCE INFLAMMATION AND
STIMULATES THE PROLIFERATION OF OSTEOBLASTS .
• ANIMAL STUDIES STRONGLY INDICATE THAT MELATONIN GEL
APPLICATION AT THE SITE OF IMPLANT PLACEMENT MAY
PROMOTE CLOSER BONE-IMPLANT CONTACT .
• SIMILAR EFFECTS OF MELATONIN ARE SEEN WHEN APPLIED
AS A GEL ON POST-EXTRACTION SOCKETS

79. • ALTHOUGH MELATONIN HAS BEEN APPROVED
BY THE FDA AS A DIETARY SUPPLEMENT FOR
TREATING SLEEP DISORDERS, THE EFFECT OF
SYSTEMIC MELATONIN ON PERIODONTAL
HEALTH AND POST-SURGICAL HEALING HAS
NOT BEEN RESEARCHED TO DATE.
• THEREFORE, FUTURE RESEARCH SHOULD
FOCUS ON THE EFFECT OF DIETARY MELATONIN
SUPPLEMENTATION ON NON-SURGICAL AND
SURGICAL PERIODONTAL THERAPY

80. DIETARY MINERALS AND TRACE
ELEMENTS
• MINERAL NUTRIENTS ARE ELEMENTS OTHER THAN OXYGEN,
CARBON, NITROGEN, AND HYDROGEN) REQUIRED BY
ORGANISMS TO SURVIVE AND FUNCTION NORMALLY.
• FOR EXAMPLE, CALCIUM, PHOSPHORUS, POTASSIUM, SULFUR,
SODIUM, CHLORINE, AND MAGNESIUM ARE NORMALLY
REQUIRED IN ABUNDANCE.
• IRON, COBALT, COPPER, ZINC, MANGANESE, MOLYBDENUM,
IODINE, BROMINE, AND SELENIUM ARE REQUIRED IN SMALL
CONCENTRATIONS AND, HENCE, ARE TERMED TRACE
MINERALS.
• DEFICIENCY OF MINERALS HAS IMPLICATIONS ON
PERIODONTAL HEALTH AS WELL.

81. CALCIUM:
• CALCIUM IS REQUIRED FOR THE NORMAL FUNCTIONING OF
MUSCLES AND BODY SYSTEMS. ADDITIONALLY, CALCIUM IS
ESSENTIAL FOR THE MAINTENANCE AND FORMATION OF
CALCIFIED TISSUES SUCH AS BONE AND TEETH.
• FURTHERMORE, IT IS ALSO REQUIRED FOR BLOOD CELLS TO
FUNCTION. DIETARY SOURCES OF CALCIUM ARE DAIRY
PRODUCTS, LEAFY VEGETABLES, NUTS, AND SEEDS.
• A LACK OF CALCIUM (HYPOCALCEMIA) MAY LEAD TO CARDIAC
ARRHYTHMIAS, CONVULSIONS, TETANY, AND NUMBNESS
AND/OR TINGLING IN HANDS, FEET AND ROUND THE LIPS.

82. • A DEFICIENCY OF DIETARY CALCIUM MAY
IMPACT PERIODONTAL HEALTH AS WELL. CO-
SUPPLEMENTATION OF CALCIUM AND VITAMIN D
IS COMMONLY USED AND HAS A POSITIVE
EFFECT ON OUTCOMES OF PERIODONTAL
THERAPY.
• IT HAS BEEN ESTABLISHED THAT LOCAL
DELIVERY OF CALCIUM, IN THE FORM OF
HYDROXYAPATITE, ENHANCES THE
OSSEOINTEGRATION OF DENTAL IMPLANTS

83. MAGNESIUM:
• MAGNESIUM IS REQUIRED FOR CELL METABOLISM
AND MAINTENANCE AND FORMATION OF BONE.
• THE DEFICIENCY OF MAGNESIUM INTERFERED WITH
THE PARATHYROID HORMONE AND DIRECTLY
AFFECTS THE BONE RESULTING IN OSTEOPOROSIS
.
• MAGNESIUM SUPPLEMENTS HAVE BEEN SHOWN TO
REDUCE INCIDENCES OF FRACTURES IN
OSTEOPOROTIC PATIENTS, INDICATING THEIR
POSITIVE EFFECT ON THE MAINTENANCE OF
BONES.

84. IRON:
• IRON IS MAINLY REQUIRED FOR SYNTHESIS OF PROTEINS,
INCLUDING HEMOGLOBIN AND ENZYMES.
• FOODS SUCH AS RED MEAT, SPINACH, FISH (TUNA AND
SALMON), AND BEANS ARE RICH SOURCES OF IRON. IRON
DEFICIENCY LEADS TO ANEMIA AND RELATED SYMPTOMS. ORAL
MANIFESTATIONS OF ANEMIA INCLUDE RECURRENT
ULCERATION, PALE MUCOSA, AND BURNING OF THE MOUTH.
• INDEED, A STUDY INDICATES THAT IRON-DEFICIENCY ANEMIA
LEADS TO A REDUCTION IN ANTIOXIDANT ENZYMES, LEADING TO
AN INCREASED OXIDATIVE STRESS AND WORSENING OF
PERIODONTAL DISEASES .
• NEVERTHELESS, NO STUDIES HAVE ATTEMPTED TO FIND A
CORRELATION BETWEEN IRON SUPPLEMENTATION AND THE
OUTCOMES OF PERIODONTAL THERAPY.

85. • PROTEIN-RICH FOODS ARE THE PRIMARY SOURCE OF
DIETARY ZINC . ZINC IS SECOND TO IRON AS THE MOST
ABUNDANTLY FOUND TRACE MINERAL IN THE HUMAN BODY.
• ZINC ACTS AS A COFACTOR IN MANY PROCESSES.
• PARTICULARLY, IT MODULATES THE PROCESSES OF AUTO-
DEBRIDEMENT AND KERATINOCYTE MIGRATION DURING
WOUND REPAIR.
• FURTHERMORE, IT ALSO EXERTS AN ANTIOXIDATIVE EFFECT
BY SCAVENGING ROS IN ADDITION TO NEUTRALIZING
BACTERIAL TOXINS.
• HENCE, ZINC IS AN IMPORTANT COMPONENT OF
PERIODONTAL DRESSINGS. DIETARY ZINC MAY ALSO PLAY AN
IMPORTANT ROLE IN MAINTAINING PERIODONTAL HEALTH.

86. FLUORIDE:
• FLUORINE PREVENTS CARIES BY STRENGTHENING ENAMEL
AND CEMENTUM DUE TO THE FORMATION OF FLUORO-
APATITE AND EXERTING AN ANTIBACTERIAL EFFECT VIA
INHIBITION OF BACTERIAL GROWTH AND ADHESION.
• FLUORIDE SUPPLEMENTATION OF 0.25 TO 1 MG PER DAY IS
RECOMMENDED DEPENDING UP ON THE PPM F ALREADY
PRESENT IN DRINKING WATER .
• ADDITIONALLY, FLUORIDE SUPPLEMENTATION MAY ALSO
REDUCE ROOT RESORPTION CAUSED BY ORTHODONTIC
MOVEMENT OF TEETH .
• GREEN TEA IS ANOTHER NUTRITIONAL SOURCE THAT IS
RICH IN VARIOUS ELEMENTS REQUIRED FOR ORAL HEALTH
INCLUDING CALCIUM, PHOSPHORUS, AND FLUORIDE

87. PROTEIN DEFICIENCY:
• PROTEIN DEPLETION RESULTS IN HYPOPROTEINEMIA WITH
MANY
PATHOLOGIC CHANGES, INCLUDING
,
.
1. muscular atrophy,
2.weakness,
3.weight loss,
4. anemia,
5. leukopenia
6. Edema
7.Impaired lactation,
8. decreased resistance
to infection
9. slow wound healing,
10. lymphoid depletion,
and
11.reduced ability to form
certain hormones and
enzyme systems

88. • PROTEIN DEPRIVATION ALSO CAUSES CHANGES
IN THE PERIODONTIUM
1.DEGENERATION OF THE CONNECTIVE TISSUE
OF THE GINGIVA AND PERIODONTAL LIGAMENT,
2.OSTEOPOROSIS OF ALVEOLAR BONE
3. RETARDATION IN THE DEPOSITION OF
CEMENTUM,
4. DELAYED WOUND HEALING,
5. AND ATROPHY OF THE TONGUE EPITHELIUM.
• SIMILAR CHANGES OCCUR IN THE PERIOSTEUM
AND BONE IN OTHER NON-ORAL AREAS.

89. • OSTEOPOROSIS RESULTS FROM REDUCED DEPOSITION
OF OSTEOID,
REDUCTION IN THE NUMBER OF OSTEOBLASTS, AND
RETARDATION
IN THE MORPHO DIFFERENTIATION OF CONNECTIVE TISSUE
CELLS TO FORM OSTEOBLASTS, RATHER THAN FROM
INCREASED
OSTEOCLASTIC ACTIVITY.
• THESE OBSERVATIONS ARE OF INTEREST IN THAT THEY
REVEAL A
LOSS OF ALVEOLAR BONE THAT IS THE RESULT OF THE
INHIBITION
OF NORMAL BONE-FORMING ACTIVITY RATHER THAN OF
THE

90. • PROTEIN DEFICIENCY ALSO ACCENTUATES THE
DESTRUCTIVE
EFFECTS OF LOCAL FACTORS AND OCCLUSAL TRAUMA ON
THE
PERIODONTAL TISSUES, BUT THE INITIATION OF GINGIVAL
INFLAMMATION AND ITS SEVERITY DEPEND ON THE LOCAL
FACTORS.
• PROTEIN DEPRIVATION RESULTS IN PERIODONTAL
TISSUES THAT
LACK INTEGRITY AND, AS A RESULT, ARE MORE
VULNERABLE TO
BREAKDOWN WHEN CHALLENGED BY BACTERIA.

91. STARVATION:
• STARVATION IS THE ULTIMATE NUTRITIONAL CHALLENGE.
WITHOUT
ANY FOOD INTAKE, THERE IS A TOTAL LACK OF NUTRIENTS, NO
PHYSICAL STIMULATION AND NO FUEL FOR ENERGY.
• PROLONGED SHOWED A REDUCTION IN PLAQUE INDEX
SCORES
AND A CONSIDERABLE INCREASE IN GINGIVAL INDEX SCORES
AS THE
FASTING PERIOD LENGTHENED.
• ACUTE STARVATION RESULTS IN OSTEOPOROSIS OF
ALVEOLAR BONE
AND OTHER BONES, REDUCTION IN THE HEIGHT OF ALVEOLAR

92. CONCLUSION:
• TO CONCLUDE , STUDIES SUGGEST THAT IMPROVING NUTRITION
AND SUPPLEMENTATION OF VITAMINS AND MINERALS, PARTICULARLY
VITAMIN C, MAY CONTRIBUTE TO IMPROVEMENT OF PERIODONTAL
HEALTH, THERE ARE A NUMBER OF LIMITATIONS OF THE CURRENT
RESEARCH THAT SHOULD BE OVERCOME. THE REPORTED TREATMENT
EFFECTS ARE TOO SMALL TO INDICATE THE MAGNITUDE OF
THERAPEUTIC
SUPPLEMENTS WHEN USED AS AN ADJUNCT TO PERIODONTAL
THERAPY.
HENCE, WELL-DESIGNED, LONG-TERM STUDIES ARE NEEDED TO
ASCERTAIN THE DIRECT EFFECTS OF DIETARY SUPPLEMENTS ON THE
OUTCOMES ON PERIODONTAL DISEASES.

93. REFRENCES:
• REVIEW:THE ROLE OF NUTRITION IN PERIODONTAL
HEALTH:AN UPDATE SHARIQ NAJEEB 1, MUHAMMAD
SOHAIL ZAFAR 2,*, ZOHAIB KHURSHID 3, SANA ZOHAIB 4
AND KHALID ALMAS 5.
• TEXT BOOK OF CLINICAL PERIODONTOLOGY- CARRANZA
• TEXT BOOK OF PERIOOBASICS
• TEXTBOOK OF CLINICAL PERIODONTICS – SHANTIPRIYA
REDDY

94. THANK YOU