role of harmones and vitamins in craniofacial growth and development

ROLE OF HORMONES AND
VITAMINS IN
CRANIOFACIAL GROWTH
AND DEVELOPMENT
Under the guidance of
Dr. Mridula Trehan
Professor and Head
Presented by Dr. Deeksha Bhanotia
First year PG
Department of Orthodontics and Dentofacial Orthopedics

CONTENTS
 INTRODUCTION
 HORMONES
 CLASSIFICATION
 FUNCTIONS
 DEFICIENCY
 ROLE OF HORMONES IN CRANIOFACIAL GROWTH AND
DEVELOPMENT
 SUPPORTING STUDIES
 VITAMINS
 CLASSIFICATION
 FUNCTIONS
 DEFICIENCY
 ROLE OF VITAMINS IN CRANIOFACIAL GROWTH AND
DEVELOPMENT
 CONCLUSION
 REFERENCES

• GROWTH
MOSS DEFINES GROWTH AS “ANY CHANGE
IN MORPHOLOGY WHICH IS WITHIN
MEASURABLE PARAMETER”
• DEVELOPMENT
MOSS STATES "DEVELOPMENT CAN BE
CONSIDERED AS A CONTINUUM OF
CAUSALLY RELATED EVENTS FROM THE
FERTILIZATION OF OVUM ONWARDS"
Premkumar S; Textbook of Craniofacial Growth(2012)1st ed page 46
INTRODUCTION

• MANY FACTORS AFFECT GROWTH BETWEEN
BIRTH AND ADULTHOOD, INCLUDING
CHROMOSOMAL ABERRATIONS, ENDOCRINE
ABNORMALITIES, BONE AND CARTILAGE
ABNORMALITIES, CHRONIC DISORDERS OF
MAIN ORGANS ETC
• HORMONES AFFECTING GROWTH INCLUDE
PITUITARY, THYROID, ADRENOCORTICAL
AND SEX HORMONES
Funatsu M , Sato K, Mitani H; Effects of Growth Hormone on Craniofacial Growth. Angle
Orthodontist:2006, Vol 76

HORMONES
DEFINITION:
“A HORMONE IS A CHEMICAL SUBSTANCE THAT IS
SECRETED INTO THE BODY FLUIDS BY ONE CELL OR A
GROUP OF CELLS AND HAS A PHYSIOLOGICAL CONTROL
EFFECT ON OTHER CELLS OF THE BODY.”
- ARTHUR C. GUYTON
TEXTBOOK OF MEDICAL PHYSIOLOGY

HORMONAL ACTION
• HORMONE DOES NOT ACT DIRECTLY ON
THE CELLULAR STRUCTURES.
• FIRST IT COMBINES WITH RECEPTORS
PRESENT ON THE TARGET CELLS AND
FORMS A HORMONE RECEPTOR
COMPLEX.
• THIS HORMONE-RECEPTOR COMPLEX
INDUCES VARIOUS CHANGES OR
REACTIONS IN THE TARGET CELLS.
Sembulingam K, Sembulingam Prema; Essentials of Medical Physiology (2012),sixth edition page

HORMONE RECEPTORS
THE HORMONE RECEPTORS ARE THE LARGE
PROTEINS PRESENT IN THE TARGET CELLS.
EACH RECEPTOR IS SPECIFIC FOR ONE SINGLE
HORMONE, i.e. EACH RECEPTOR CAN COMBINE
WITH ONLY ONE HORMONE.
Sembulingam K, Sembulingam Prema; Essentials of Medical Physiology (2012),sixth edition

Sembulingam K, Sembulingam Prema; Essentials of Medical Physiology (2012),6th ed page no.369

ROLE OF HORMONES IN
CRANIOFACIAL GROWTH AND
DEVELOPMENT

PITUITARY GLAND
• PITUITARY GLAND OR HYPOPHYSIS IS A SMALL
ENDOCRINE GLAND WITH A DIAMETER OF 1 CM
AND WEIGHT OF 0.5 TO 1 G.
IT IS SITUATED IN A DEPRESSION CALLED ‘SELLA
TURCICA’,
PRESENT IN THE SPHENOID BONE AT THE BASE OF
SKULL.
DIVISIONS OF PITUITARY GLAND
PITUITARY GLAND IS DIVIDED INTO TWO DIVISIONS:
1. ANTERIOR PITUITARY OR ADENOHYPOPHYSIS
2. POSTERIOR PITUITARY OR NEUROHYPOPHYSIS

ANTERIOR PITUITARY OR ADENOHYPOPHYSIS
 ANTERIOR PITUITARY IS ALSO KNOWN AS
THE MASTER GLAND BECAUSE IT
REGULATES MANY OTHER ENDOCRINE
GLANDS THROUGH ITS HORMONES.
 CONTROLS AND STIMULATES GROWTH
AND DEVELOPMENT OF BODY IN GENERAL.
Sembulingam K, Sembulingam Prema; Essentials of Medical Physiology (2012),sixth
edition page no.376

GROWTH HORMONE
• ALSO CALLED AS SOMATOTROPHIC HORMONE
(STH) OR SOMATOTROPIN
• GH IS RESPONSIBLE FOR THE GROWTH OF
ALMOST ALL TISSUES OF THE BODY, WHICH ARE
CAPABLE OF GROWING.
• IT INCREASES THE SIZE AND NUMBER OF CELLS
BY MITOTIC DIVISION.
• GH ALSO CAUSES SPECIFIC DIFFERENTIATION OF
CERTAIN TYPES OF CELLS LIKE BONE CELLS AND
MUSCLE CELLS.
Sembulingam K, Sembulingam Prema; Essentials of Medical Physiology (2012),sixth edition page no.376

GROWTH HORMONE INCREASES:
I. SYNTHESIS AND DEPOSITION OF PROTEINS BY
CHONDROCYTES AND OSTEOGENIC CELLS.
II. MULTIPLICATION OF CHONDROCYTES AND
OSTEOGENIC CELLS BY ENHANCING THE INTESTINAL
CALCIUM ABSORPTION.
III. FORMATION OF NEW BONES BY CONVERTING
CHONDROCYTES INTO OSTEOGENIC CELLS.
IV. AVAILABILITY OF CALCIUM FOR MINERALIZATION OF
BONE MATRIX.

• GROWTH HORMONE INCREASES THE
LENGTH OF THE BONES, UNTIL EPIPHYSIS
FUSES WITH SHAFT, WHICH OCCURS AT THE
TIME OF PUBERTY.
• AFTER THE EPIPHYSEAL FUSION, LENGTH OF
THE BONES CANNOT BE INCREASED.
• HOWEVER, GH STIMULATES THE
OSTEOBLASTS STRONGLY. SO, THE BONE
CONTINUES TO GROW IN THICKNESS
THROUGHOUT THE LIFE.
• PARTICULARLY, THE MEMBRANOUS BONES
SUCH AS THE JAW BONE AND THE SKULL
BONES BECOME THICKER UNDER THE
INFLUENCE OF GH.

SOMATOMEDIN
• SOMATOMEDIN IS A SUBSTANCE THROUGH WHICH
GROWTH HORMONE ACTS.
• IT IS A POLYPEPTIDE WITH THE MOLECULAR WEIGHT OF
ABOUT 7,500
• GH ACTS ON BONES, GROWTH AND PROTEIN
METABOLISM THROUGH SOMATOMEDIN SECRETED BY
LIVER. GH STIMULATES THE LIVER TO SECRETE
SOMATOMEDIN.
• SOMETIMES, IN SPITE OF NORMAL SECRETION OF GH,
GROWTH IS ARRESTED (DWARFISM) DUE TO THE
ABSENCE OR DEFICIENCY OF SOMATOMEDIN.

CONTROL OF MAXILLARY GROWTH BY STH
GROWTH HORMONE (STH) AND SOMATOMEDIN AS
WELLAS TESTOSTERONE AND ESTROGEN ARE SEEN TO
PLAY A PRIMARY ROLE IN THE EXTRINSIC CONTROL OF
POSTNATAL GROWTH OF THE UPPER JAW- AND THERE
EFFECT IS BY DIRECT AND INDIRECT STIMULATING
ACTION.
- STUTZMANN AND PETROVIC 1976
Graber M, Rakosi T, petrovic G; dentofacial orthopedics with functional appliances(1985), page
no.27

DIRECT EFFECT
• THE DIRECT EFFECT REPRESENTS ALMOST THE
ENTIRE INFLUENCE OF STH-SOMATOMEDIN ON
GROWTH OF SPHENO-OCCIPITAL
SYNCHONDROSIS AND NASAL SEPTAL
CARTILAGE, THE LATERAL MASSES OF
ETHMOID BONE, AND BETWEEN BODY OF
GREATER WINGS OF SPHENOID.
• SMALL EFFECT ON THE GROWTH OF CRANIAL
AND FACIAL SUTURES IS OF DIRECT NATURE
Graber M, Rakosi T, petrovic G; dentofacial orthopedics with functional

INDIRECT EFFECT
THE INDIRECT EFFECT OF STH-SOMATOMEDIN OCCURS
THROUGH A NUMBER OF INTERMEDIARIES.
 FORWARD GROWTH OF NASAL SEPTAL CARTILAGE
• PRODUCES FORWARD SHIFT OF PREMAXILLARY BONE
WHICH LEADS TO INCREASE IN GROWTH OF
PREMAXILLOMAXILLARY SUTURE.
• RESULTS IN FORWARD TRACTION OF
SEPTOPREMAXILLARY LIGAMENT AND
LABIONARINARY MUSCLES RESULTING IN FORWARD
GROWTH OF THE PREMAXILLA.

OUTWARD GROWTH
• OUTWARD GROWTH OF LATERAL CARTILAGINOUS
MASSES OF THE ETHMOID AND CARTILAGE BETWEEN
BODY AND GREATER WINGS OF SPHENOID BRINGS
ABOUT A LATERALIZATION OF THE ALVEOLAR RIDGES
ON BOTH THE LEFT AND RIGHT SIDE AND, IN TURN,
STIMULATES THE GROWTH OF MID-PALATAL SUTURE.
Graber M, Rakosi T, petrovic G; dentofacial orthopedics with functional appliances(1985),
page no.30

CONTROL OF MANDIBULAR GROWTH BY STH
• STH-SOMATOMEDIN STIMULATES GROWTH OF
CONDYLAR CARTILAGE, CORONOID AND
ANGULAR CARTILAGE OF THE MANDIBLE.
• GROWTH OF THE CONDYLAR CARTILAGE HAS
AN EFFECT ON THE MANDIBULAR ANGLE.
• THE MANDIBULAR ANGLE ALONG WITH THE
APPOSITIONAL GROWTH OF POSTERIOR
BORDER OF RAMUS, CONTROLS THE FORWARD
GROWTH OF MANDIBLE.

SUPPORTING STUDIES
 EFFECTS OF GROWTH HORMONE ON
CRANIOFACIAL GROWTH
FIFTY-SEVEN PATIENTS (33 BOYS AND 24 GIRLS,
AGE RANGE 4.5 TO 16.7 YEARS) WITH GHD WERE
INVESTIGATED AND CATEGORIZED INTO THREE
GROUPS ACCORDING TO THE DURATION OF GH
THERAPY: THE UNTREATED GROUP, THE SHORT-
TERM THERAPY GROUP, AND THE LONG-TERM
THERAPY GROUP. THEIR LATERAL
CEPHALOMETRIC RADIOGRAPHS WERE
STUDIED, AND CRANIOFACIAL MEASUREMENTS
WERE ASSESSED.
Orthodontist:2006, Vol 76

• CONCLUSIONS:
CHILDREN WHO RECEIVED LONG-TERM GH
REPLACEMENT THERAPY SHOWED INCREASED
GROWTH OF THE CRANIOFACIAL SKELETON,
ESPECIALLY THE MAXILLAAND RAMUS.
THESE FINDINGS SUGGEST THAT GH
ACCELERATES CRANIOFACIAL DEVELOPMENT,
WHICH IMPROVES OCCLUSION AND THE FACIAL
PROFILE.

 DIFFERENTIAL GROWTH AND MATURATION
IN IDIOPATHIC GROWTH-HORMONE-
DEFICIENT CHILDREN
THIS STUDY DESCRIBES AND COMPARES THE
GROWTH AND MATURATION OF IDIOPATHIC
GROWTH HORMONE DEFICIENCY (IGHD) AND
EVALUATES THE POTENTIAL EFFECTS OF GROWTH
HORMONE THERAPY. THE SAMPLE INCLUDES 40
IDIOPATHIC GROWTH-HORMONE-DEFICIENT
CHILDREN GROUPED ACCORDING TO DURATION
OF GROWTH HORMONE REPLACEMENT THERAPY.
Cantu G, Buschang H, Gonzalez JL; Differential growth and maturation in idiopathic growth-hormone-
deficient children, European Journal of Orthodontics (1997)

• CONCLUSION:
CATCH-UP GROWTH FOLLOWING GH THERAPY
APPEARS TO BE MOST PRONOUNCED FOR HEIGHT,
FACIAL HEIGHT, SKELETAL AGE AND POSTERIOR
CRANIAL BASE LENGTH.
Cantu G, Buschang H, Gonzalez JL; Differential growth and maturation in idiopathic growth-hormone-
deficient children, European Journal of Orthodontics (1997)

INFLUENCE OF GROWTH HORMONE ON THE
CRANIOFACIAL COMPLEX OF TRANSGENIC MICE
• THIS STUDY INVESTIGATED THE EFFECT OF GH ON
THE SIZE OF THE CRANIOFACIAL STRUCTURES AND
THEIR ANGULAR RELATIONSHIP.
• THREE DIFFERENT MODELS OF MICE WITH A
GENETICALLY ALTERED GH AXIS WERE USED:
1. GH EXCESS (GIANT),
2. DWARF GH ANTAGONIST (DWARF-ANT),
3. DWARF GH RECEPTOR KNOCKOUT (DWARF-KO)
MICE.
Ramirez-Yanez, Smid J, Young WG, Waters MJ;Influence of growth hormone on the craniofacial
complex of transgenic mice, European Journal of Orthodontics (2005)

• CONCLUSIONS
THE RESULTS OF THIS STUDY SHOW THAT THE SIZE
OF THE CRANIOFACIAL STRUCTURES AND THEIR
ANGULAR RELATIONSHIPS ARE DIRECTLY LINKED TO
GH STATUS.
DIFFERENCES WERE PARTICULARLY FOUND
BETWEEN THE THREE GH GENETICALLY MODIFIED
MICE IN:
• THE LENGTH OF BOTH MAXILLARYAND
MANDIBULAR INCISORS
• THE SIZE OF THE CRANIOFACIAL BONES
• THE LENGTH OF THE MANDIBULAR CORPUS AND
RAMUS
Ramirez-Yanez, Smid J, Young WG, Waters MJ;Influence of growth hormone on the craniofacial complex
of transgenic mice, European Journal of Orthodontics (2005)

HYPOFUNCTION OF THE PITUITARY GLAND
DWARFISM
• DWARFISM RESULTS FROM GENERALIZED
DEFICIENCY OF ANTERIOR PITUITARY
SECRETION DURING CHILDHOOD.
• IN GENERAL, ALL THE PHYSICAL PARTS OF
THE BODY DEVELOP IN APPROPRIATE
PROPORTION TO ONE ANOTHER, BUT THE
RATE OF DEVELOPMENT IS GREATLY
DECREASED.
Guyton AC, Hall JE; Textbook of Medical Physiology (2011) twelfth edition pg

• THE DENTOFACIAL CHANGES
• DELAYED TOOTH ERUPTION
• RETARTED JAW GROWTH - SMALL VERTICAL
DIMENSION AND A SMALL ARCH LENGTH
• MANDIBULAR TOTAL LENGTH IS REDUCED
• CROWDING AND MALOCCLUSION DUE TO
DISPROPORTION IN SIZE OF JAWS AND
TEETH.
• TEETH HAVE SHORT ROOTS, WIDE PULP
CHAMBER AND WIDE APICAL FORAMINA.
Ghom A, Ghom S; Textbook of oral radiology,(2016),second edition, page no. 754

HYPERFUNCTION OF THE PITUITARY GLAND
GIGANTISM
• PITUITARY DISORDER CHARACTERIZED
BY EXCESS GROWTH OF THE BODY.
• DUE TO HYPERSECRETION OF GH IN
CHILDHOOD OR IN PRE-ADULT LIFE
BEFORE THE FUSION OF EPIPHYSIS OF
BONE WITH SHAFT.

CLINICAL FEATURES
• GENERAL OVERGROWTH - WITH A HEIGHT OF
MORE THAN 7 OR 8 FEET.
• THE LIMBS ARE DISPROPORTIONATELY LONG
• BROAD, ENLARGED NOSE AND PROGNATHIC
MANDIBLE
• THE PATIENT MAY DEVELOP CLASS III
MALOCCLUSION
• HYPERCEMENTOSIS
• THE TEETH IN GIGANTISM ARE
PROPORTIONAL TO THE SIZE OF THE JAWS
AND THE REST OF THE BODY.
• THE ROOTS MAY BE LONGER THAN NORMAL.
Shafer, Hine, Levy; Textbook of Oral Pathology(2020) ninth edition page no 2491

ACROMEGALY
DISORDER CHARACTERIZED BY THE
ENLARGEMENT, THICKENING AND
BROADENING OF BONES, PARTICULARLY
IN THE EXTREMITIES OF THE BODY.
DUE TO HYPERSECRETION OF GH IN
ADULTS AFTER THE FUSION OF EPIPHYSIS
WITH SHAFT OF THE BONE.

THE DENTOFACIAL CHANGES
• OVERGROWTH OF CONDYLE OCCURS - LEADS
TO FORWARD POSITIONING OF
MANDIBLE(PROGNATHISM).
• MACROGLOSSIA - CAUSE PRESSURE ON THE
TEETH AND SEPARATION OF THE TEETH
OCCURS - RESULTS IN SPACING BETWEEN THE
TEETH.
• INDENTATION ALSO OCCURS ON THE LATERAL
BORDER OF TONGUE DUE TO PRESSURE OF
TEETH.
• THERE ARE PROBLEMS WITH FITTING OF
DENTURE AS ENLARGEMENT OF ALVEOLUS
CAN OCCUR.
Ghom A, Ghom S; Textbook of oral radiology,(2016),second edition, page no.

THYROID GLAND
• LOCATED IMMEDIATELY BELOW THE
LARYNX ON EACH SIDE OF AND ANTERIOR
TO THE TRACHEA
• ONE OF THE LARGEST OF THE ENDOCRINE
GLANDS -15 TO 20 GRAMS IN ADULTS.
• THE THYROID SECRETES THREE MAJOR
HORMONE
 TETRAIODOTHYRONINE OR THYROXINE (T4)
 TRIIODOTHYRONINE (T3)
CALCITONIN

THYROID HORMONE
IT PLAYS AN ESSENTIAL ROLE IN:
• DIFFERENTIATION, GROWTH, MATURATION
• WATER BALANCE
• ELECTROLYTE BALANCE,
• PROTEIN STORAGE
• CARBOHYDRATE AND LIPID METABOLISM,
• OTHER PHYSIOLOGIC FUNCTIONS.
Shafer, Hine, Levy; Textbook of Oral Pathology(2020) ninth edition page no
2493

HYPOTHYROIDISM
DECREASED SECRETION OF THYROID
HORMONES IS CALLED HYPOTHYROIDISM.
IF THIS OCCURS IN INFANCY, IT MAY RESULT
IN CRETINISM -WHICH LEADS TO
 MENTAL DEFECTS,
 RETARDED SOMATIC GROWTH
 GENERALIZED EDEMA
AND OTHER CHANGES, DEPENDING ON THE
SEVERITY OF THE DEFICIENCY OF THYROID
HORMONE
Cretinism (3-month-old
baby
Shafer, Hine, Levy; Textbook of Oral Pathology(2020) ninth edition

THE DENTOFACIAL CHANGES :
• SPHENOID BONE IS STUNTED, ESPECIALLY AT
SPHENO-OCCIPITAL SUTURE
• THE BASE OF THE SKULL IS SHORTENED,
LEADING TO A RETRACTION OF THE BRIDGE OF
THE NOSE WITH FLARING.
• THE FACE IS WIDE AND FAILS TO DEVELOP IN A
LONGITUDINAL DIRECTION.
• OSSIFICATION OF CARTILAGE CENTERS IS
DELAYED
• THE MANDIBLE IS UNDERDEVELOPED AND THE
MAXILLA IS OVERDEVELOPED.
Shafer, Hine, Levy; Textbook of Oral Pathology(2020) ninth edition

IF IT OCCURS IN CHILDHOOD, JUVENILE
MYXEDEMA OCCURS.
• IN JUVENILE HYPOTHYROIDISM, THE
TONGUE IS ENLARGED BY EDEMA FLUID,
IT MAY PROTRUDE CONTINUOUSLY AND
LEAD TO MALOCCLUSION.
• THE ERUPTION RATE OF THE TEETH IS
DELAYED
• ABNORMAL DENTAL CALCIFICATION AND
ROOT RESORPTION
• THE DECIDUOUS TEETH ARE RETAINED
BEYOND THE NORMAL SHEDDING TIME
• OSTEOPOROTIC CONDITION IN ALVEOLAR
BONE
Shafer, Hine, Levy; Textbook of Oral Pathology(2020) ninth edition page

IF IT OCCURS IN THE ADULT, IT LEADS TO
MYXEDEMA
• THE CLINICAL OROFACIAL FINDINGS IN
MYXEDEMATOUS PATIENTS ARE
APPARENTLY LIMITED TO THE SOFT TISSUES
OF THE FACE AND MOUTH.
• THE LIPS, NOSE, EYELIDS, AND SUBORBITAL
TISSUES ARE EDEMATOUS AND SWOLLEN.
• THE TONGUE IS LARGE AND EDEMATOUS,
FREQUENTLY INTERFERING WITH SPEECH.
2494

HYPERTHYROIDISM
INCREASED SECRETION OF THYROID HORMONES
IS CALLED HYPERTHYROIDISM
• THERE ARE TWO FUNDAMENTALLY DIFFERENT
TYPES OF HYPERTHYROIDISM:
• EXOPHTHALMIC GOITER , CHARACTERIZED BY
DIFFUSE HYPERPLASIA OF THE THYROID AND BY
EYE SIGNS
• TOXIC ADENOMA , IN WHICH HYPERFUNCTION
ORIGINATES IN A BENIGN TUMOR OF THE
THYROID GLAND

CLINICAL FEATURES
• IN CHILDREN, SHEDDING OF THE
DECIDUOUS TEETH OCCURS EARLIER THAN
NORMAL, AND ERUPTION OF THE
PERMANENT TEETH IS GREATLY
ACCELERATED
• THE MOST COMMON CRANIOFACIAL
MANIFESTATION OF HYPERTHYROIDISM IS
PREMATURE FUSION OF THE SUTURES
• INCREASED RISK OF DEVELOPMENT OF
PERIODONTAL DISEASE AND CARIES
• OSTEOPOROSIS OF MAXILLAAND MANDIBLE
• INCREASED RISK OF DENTAL EROSION
Leitch V,Bassett D,Williams G; Role of thyroid hormones in craniofacial development,2020
Burkhart NW, Delong L; General and oral pathology for dental hygienist,(2008)first edition ,page
no 158

CALCITONIN
• CALCITONIN INHIBITS BONE RESORPTION
BY DIRECT ACTION ON OSTEOCLASTS
• IT ALSO STIMULATES THE ACTIVITY OF
OSTEOBLASTS.
• CALCITONIN ALONG WITH VITAMIN-D AND
PARATHYROID HORMONE REGULATE THE
AMOUNT OF CALCIUM AND PHOSPHORUS
Dr. Priyanka paria, Dr. renuka patel, Dr. falguni Mehta; role of nutrition and hormone in
orthodontics (2020)vol 7

PARATHYROID GLAND
• HUMAN BEINGS HAVE FOUR
PARATHYROID GLANDS, WHICH ARE
SITUATED ON THE POSTERIOR SURFACE
OF UPPER AND LOWER POLES OF
THYROID GLAND
• EACH PARATHYROID GLAND IS MADE UP
OF CHIEF CELLS AND OXYPHIL CELLS.
• CHIEF CELLS SECRETE PARATHORMONE
(PTH)
edition page no.400

PARATHORMONE
• PARATHYROID GLAND RELEASE
PARATHORMONE THAT MAINTAINS
PLASMA IONIZED CALCIUM LEVEL.
• IONIZED CALCIUM IS ESSENTIAL
FOR BONE AND TOOTH
DEVELOPMENT
no 2495

HYPERPARATHYROIDISM
HYPERSECRETION OF PTH IS CALLED
HYPERPARATHYROIDISM.
IT RESULTS IN HYPERCALCEMIA.
HYPERPARATHYROIDISM IS OF TWO TYPES:
1. PRIMARY HYPERPARATHYROIDISM
2. SECONDARY HYPERPARATHYROIDISM

PRIMARY HYPERPARATHYROIDISM
• PRIMARY HYPERPARATHYROIDISM IS DUE TO
THE DEVELOPMENT OF TUMOR IN ONE OR
MORE PARATHYROID GLANDS.
• SOMETIMES, TUMOR MAY DEVELOP IN ALL
THE FOUR GLANDS.
• THE FIRST SIGN OF THE DISEASE MAY BE A
GIANT CELL TUMOR OR A “CYST” OF THE
JAW
• MALOCCLUSION CAUSED BY A SUDDEN
DRIFTING WITH DEFINITE SPACING OF THE
TEETH MAY BE SEEN

• LOSS OF PHOSPHORUS AND
CALCIUM RESULTS IN A
GENERALIZED OSTEOPOROSIS
• LARGE OR SMALL SHARPLY
DEFINED RADIOLUCENCIES MAY
BE PRESENT IN THE MAXILLA
AND/OR MANDIBLE
• LAMINA DURAAROUND THE
TEETH MAY BE PARTIALLY LOST

SECONDARY HYPERPARATHYROIDISM
• IN SECONDARY HYPERPARATHYROIDISM,
HIGH LEVELS OF PTH OCCUR AS A
COMPENSATION FOR HYPOCALCEMIA
RATHER THAN AS A PRIMARY ABNORMALITY
OF THE PARATHYROID GLANDS
• THIS CONTRASTS WITH PRIMARY
HYPERPARATHYROIDISM, WHICH IS
ASSOCIATED WITH HYPERCALCEMIA
• ASSOCIATED WITH CHRONIC KIDNEY
DISEASE
Guyton AC, Hall JE; Textbook of Medical Physiology (2011) twelfth edition pg 968

HYPOPARATHYROIDISM
• HYPOSECRETION OF PTH IS CALLED
HYPOPARATHYROIDISM.
• IT LEADS TO HYPOCALCEMIA (DECREASE IN
BLOOD CALCIUM LEVEL)
• PATIENTS WILL HAVE INCREASED
NEUROMUSCULAR EXCITABILITY,
RESULTING IN MUSCLE SPASMS, STIFFNESS,
CRAMPING, AND TETANY.

SPECIFIC ORAL MANIFESTATIONS
INCLUDE
• ALTERED TOOTH ERUPTION
PATTERN
• SHORT, BLUNTED ROOTS
• ENAMEL HYPOPLASIA
• DENTIN DYSPLASIA
• IMPACTED TEETH
• PARTIALANODONTIA.
• ABNORMAL TOOTH NUMBER

ADRENAL GLAND
• THERE ARE TWO ADRENAL GLANDS.
• EACH GLAND IS SITUATED ON THE
UPPER POLE OF EACH KIDNEY.
• BECAUSE OF THE SITUATION
ADRENAL GLANDS ARE OTHERWISE
CALLED SUPRARENAL GLANDS.
• EACH GLAND WEIGHS ABOUT 4 G

• ADRENAL GLANDS ARE CALLED THE
‘LIFE-SAVING GLANDS’ OR
‘ESSENTIAL ENDOCRINE GLANDS’.
• IT IS BECAUSE THE ABSENCE OF
ADRENOCORTICAL HORMONES CAUSES
DEATH WITHIN 3 TO 15 DAYS
• ABSENCE OF ADRENOMEDULLARY
HORMONES, DRASTICALLY DECREASES
THE RESISTANCE TO MENTAL AND
PHYSICAL STRESS.

ADRENAL GLAND IS MADE OF TWO DISTINCT
PARTS:
1. ADRENAL CORTEX: OUTER PORTION,
CONSTITUTING 80% OF THE GLAND
2. ADRENAL MEDULLA: CENTRAL PORTION,
CONSTITUTING 20% OF THE GLAND.

HORMONES OFADRENAL CORTEX
ADRENOCORTICAL HORMONES ARE STEROIDS IN
NATURE. BASED ON THEIR FUNCTIONS, THEY ARE
CLASSIFIED INTO THREE GROUPS:
1. MINERALOCORTICOIDS
2. GLUCOCORTICOIDS
3. SEX HORMONES

ADRENOCORTICAL INSUFFICIENCY OR ADDISON'S DISEASE
• CHRONIC DISEASE THAT OCCURS WHEN
CORTICAL HORMONES ARE DEFICIENT AND
ADRENOCORTICOTROPIC HORMONE LEVELS
ARE ELEVATED
• IT USUALLY DEVELOPS FOLLOWING THE
AUTOIMMUNE DESTRUCTION OF ADRENAL
GLANDS AND FREQUENTLY OCCURS IN
CONJUNCTION WITH OTHER AUTOIMMUNE
DISORDERS.
Burkhart NW, Delong L; General and oral pathology for dental hygienist,(2008)first edition ,page no
159

• EARLY MANIFESTATIONS INCLUDE LETHARGY, FATIGUE,
AND MUSCULAR WEAKNESS
• THE PATIENT FEELS TIRED AFTER MINIMAL EXERTION BUT
FEELS WELL ON WALKING
• VOMITING, DIARRHEA, AND SEVERE ANEMIAARE ALSO
SEEN
• FEMALES DEVELOP IRREGULAR MENSTRUATION AND LOSS
OF BODY HAIR
• HYPOGLYCAEMIA, DEHYDRATION, HYPERTENSION,
ELEVATED SERUM POTASSIUM, AND POSTURAL DIZZINESS
DEVELOP LOW BLOOD LEVELS OF CORTISOL

• IN THE ORAL MUCOSA, A PALE
BROWN TO DEEP CHOCOLATE
PIGMENTATION SPREADING OVER THE
BUCCAL MUCOSA FROM THE ANGLES
OF THE MOUTH AND/OR DEVELOPING
ON THE GINGIVA, TONGUE, AND LIPS
MAY BE THE FIRST EVIDENCE OF THE
DISEASE

HYPERADRENALISM (CUSHING DISEASE)
• THIS SYNDROME IS A RESULT OF
HORMONAL EXCESS RESULTING FROM
ANY OF THE FOLLOWING:
1. HYPERPLASTIC ADRENAL CORTICES
WITHOUT ANY OTHER CLINICALLY
EVIDENT ENDOCRINE LESION
2. 2. ADRENAL CORTICAL ADENOMA OR
CARCINOMA ECTOPICALLY LOCATED
ADRENAL-LIKE TUMOR, FOR EXAMPLE,
OF AN OVARY

3. ACTH-SECRETING TUMOR OF THE ANTERIOR
PITUITARYASSOCIATED WITH ADRENAL CORTICAL
HYPERPLASIA
4. NONPITUITARY CARCINOMA, FOR EXAMPLE, OF A
LUNG OR THE PANCREAS, WITH SECRETION OF AN
ACTH-LIKE MATERIAL THAT INDUCES ADRENAL
CORTICAL HYPERPLASIA

CLINICAL FEATURES
• FAT IN ABDOMEN, ABOVE THE CLAVICLES AND IN
UPPER BACK (BUFFALO HUMP)
• THINNING OR ATROPHY OF SKIN
• RAPID WEIGHT GAIN
• EXHIBIT STEROID ACNE (FACE, CHEST, UPPER
BODY)
• COLLAGEN DEFICIENCIES CAUSE PURPLE STRIAE,
OR STRETCH MARKS TO FORM OVER ABDOMEN,
UPPER ARMS, UPPER THIGHS AND BREASTS
• LONG TERM DISEASE CAN LEAD TO
OSTEOPOROSIS, DIABETES MELLITUS, STOMACH
ULCER
Burkhart NW, Delong L; General and oral pathology for dental hygienist,(2008)first edition ,page no

PERIORAL AND INTRAORAL CHARACTERISTICS
• ROUND FULL FACE (MOON FACE)
CAUSED BY EDEMA
• RISK OF DEVELOPING ORAL AND
OROPHARYNGEAL FUNGAL INFECTIONS
• CANDIDAALBICANS IS THE MOST
COMMON CAUSE OF INFECTION
Burkhart NW, Delong L; General and oral pathology for dental hygienist,(2008)first edition ,page
no 162

CORTICOSTEROIDS
• CORTICOSTEROIDS ARE MAN-MADE DRUGS
THAT CLOSELY RESEMBLE CORTISOL
• CORTICOSTEROIDS ARE OFTEN REFERRED
TO BY THE SHORTENED TERM "STEROIDS”
• CORTICOSTEROIDS ARE
IMMUNOSUPPRESSIVE AND ANTI-
INFLAMMATORYAGENTS
Dr. Priyanka paria, Dr. renuka patel, Dr. falguni Mehta; role of nutrition and hormone in orthodontics

EFFECTS ON BONE AND TOOTH MOVEMENT
• EVIDENCE INDICATES THAT THE MAIN EFFECT OF
CORTICOSTEROIDS ON BONE TISSUE IS DIRECT
INHIBITION OF OSTEOBLASTIC FUNCTION AND
THUS THE DECREASE OF TOTAL BONE FORMATION.
• CORTICOSTEROIDS INCREASE THE RATE OF
TOOTH MOVEMENT
• SINCE NEW BONE FORMATION CAN BE DIFFICULT
IN TREATED PATIENTS, THEY DECREASE THE
STABILITY OF TOOTH MOVEMENT AND STABILITY
OF ORTHODONTIC TREATMENT IN GENERAL

GONADS
• TESTIS
1. TESTOSTERONE
2. DIHYDROTESTOSTERONE
3. ANDROSTENEDION
• OVARY
1. ESTROGEN
2. PROGESTERONE

ROLE OF SEX HORMONES
• GH AND TESTOSTERONE CONTRIBUTE TO
MANDIBULAR GROWTH
• KELLER, SATHER AND HAYLES REPORTED
DELAYED FACIAL GROWTH IN
HYPOGONADISM
• ESTROGEN DIRECTLY STIMULATES THE
BONE-FORMING ACTIVITY OF OSTEOBLASTS.

• ESTROGEN AND ANDROGENS INHIBIT BONE
RESORPTION AND MODULATE THE GROWTH
OF THE MUSCULAR SYSTEM
• SEVERAL STUDIES HAVE SHOWN THAT
ESTROGEN DEFICIENCY ACCELERATED
TOOTH MOVEMENT
• ESTROGEN INHIBITS TOOTH MOVEMENT BY
INCREASING THE BONE MINERAL CONTENT
AND BONE MASS AND BY REDUCING THE
BONE RESORPTION RATE.

SUPPORTING STUDIES
EFFECT OF LOW-DOSE TESTOSTERONE TREATMENT
ON CRANIOFACIAL GROWTH IN BOYS WITH
DELAYED PUBERTY
• CRANIOFACIAL GROWTH WAS INVESTIGATED IN
BOYS TREATED WITH LOW-DOSE TESTOSTERONE
FOR DELAYED PUBERTY AND COMPARED WITH
CONTROLS. AT THE BEGINNING OF THE STUDY,
STATURAL HEIGHT, MANDIBULAR RAMUS
LENGTH, UPPER ANTERIOR FACE HEIGHT, AND
TOTAL CRANIAL BASE LENGTH WERE
SIGNIFICANTLY SHORTER IN THE DELAYED
PUBERTY BOYS.
Verdonck A, Gaethofs M, Carels C, Zegher F; Effect of low-dose testosterone treatment on
craniofacial growth in boys with delayed puberty, European journal of orthodontics (1999)

• AFTER 1 YEAR, THE GROWTH RATE OF THE
STATURAL HEIGHT, TOTAL MANDIBULAR
LENGTH, RAMUS LENGTH, AND UPPER AND
TOTAL ANTERIOR FACE HEIGHT WAS
SIGNIFICANTLY HIGHER IN THE TREATED BOYS.
CONCLUSION:
• LOW DOSES OF TESTOSTERONE ACCELERATE
STATURAL AND CRANIOFACIAL GROWTH,
PARTICULARLY IN THE DELAYED COMPONENTS,
THUS LEADING TOWARDS A NORMALIZATION OF
FACIAL DIMENSIONS.
Verdonck A, Gaethofs M, Carels C, Zegher F; Effect of low-dose testosterone treatment on
craniofacial growth in boys with delayed puberty, European journal of orthodontics (1999)

VITAMINS
VITAMINS MAY BE REGARDED AS ORGANIC
COMPOUNDS REQUIRED IN THE DIET IN
SMALLAMOUNTS TO PERFORM SPECIFIC
BIOLOGICAL FUNCTIONS FOR NORMAL
MAINTENANCE OF OPTIMUM GROWTH AND
HEALTH OF THE ORGANISM.
Satyanarayana U,Chakrapani U; Biochemistry(2013),Fourth edition, page no 116

CLASSIFICATION
Shaik PS, Pachava S; The Role of Vitamins and Trace Elements on Oral Health International Journal of Medical Reviews
(2017)

FAT SOLUBLE VITAMINS
• THE FOUR VITAMINS, NAMELY VITAMIN A, D, E,
AND K ARE KNOWN AS FAT OR LIPID SOLUBLE.
• THEY ARE SOLUBLE IN FATS AND
• FAT SOLUBLE VITAMINS CAN BE STORED IN LIVER
AND ADIPOSE TISSUE.
• THEY ARE NOT READILY EXCRETED IN URINE.
• EXCESS CONSUMPTION OF THESE VITAMINS
(PARTICULARLY AAND D) LEADS TO THEIR
ACCUMULATION AND TOXIC EFFECTS.

VITAMIN A
• THE ACTIVE FORM IS PRESENT ONLY IN ANIMAL
TISSUES.
• ITS PROVITAMIN, BETA-CAROTENE IS PRESENT IN
PLANT TISSUES.
• THE TERM RETINOIDS IS OFTEN USED TO
INCLUDE THE NATURAL AND SYNTHETIC FORMS
OF VITAMIN A. RETINOL, RETINAL AND
RETINOIC ACID ARE REGARDED AS VITAMERS
OF VITAMIN A.

DIETARY SOURCES
• ANIMAL SOURCES CONTAIN (PREFORMED)
VITAMIN A.
THE BEST SOURCES ARE LIVER, KIDNEY, EGG YOLK,
MILK, CHEESE, BUTTER.
FISH (COD OR SHARK) LIVER OILS ARE VERY RICH IN
VITAMIN A.
• VEGETABLE SOURCES CONTAIN THE PROVITAMIN
A-CAROTENES.
YELLOW AND DARK GREEN VEGETABLES AND
FRUITS ARE GOOD SOURCES OF CAROTENES
e.g.CARROTS, SPINACH, PUMPKINS, MANGO, PAPAYA
ETC.

RECOMMENDED DIETARY ALLOWANCE (RDA)
• THE RDA OF VITAMIN A FOR ADULTS
IS:
1,000 RETINOL EQUIVALENTS (3,500 IU)
FOR MAN
800 RETINOL EQUIVALENTS (2,500 IU)
FOR WOMAN
• THE REQUIREMENT INCREASES IN
PREGNANT AND LACTATING MOTHERS

FUNCTIONS OF VITAMIN A
• REGULATE THE PROTEIN SYNTHESIS
AND THUS ARE INVOLVED IN THE
CELL GROWTH AND
DIFFERENTIATION.
• HELPS IN VISION
• MAINTAIN HEALTHY EPITHELIAL
TISSUE.

• RETINOL IS NECESSARY FOR NORMAL
REPRODUCTION.
• MAINTENANCE OF PROPER IMMUNE
SYSTEM
• CHOLESTEROL SYNTHESIS.
• CAROTENOIDS FUNCTION AS
ANTIOXIDANTS.
• PREVENT HEART ATTACKS

VITAMIN A DEFICIENCY
• NIGHT BLINDNESS
• SEVERE DEFICIENCY LEADS TO
XEROPHTHALMIA
• IF XEROPHTHALMIA PERSISTS FOR A LONG
TIME, CORNEAL ULCERATION AND
DEGENERATION OCCUR-KERATOMALACIA
• THE SKIN BECOMES ROUGH AND DRY.

• DEGENERATION OF GERMINAL EPITHELIUM
LEADS TO STERILITY IN MALES
• GROWTH RETARDATION DUE TO IMPAIRMENT
IN SKELETAL FORMATION
• ORAL MANIFESTATIONS
• VITAMIN A DEFICIENCY LEADS TO SPECIFIC
ABNORMALITIES IN THE SHAPE AND
STRUCTURE OF TEETH DURING
DEVELOPMENT
• VITAMIN-A DEFICIENCY MAY BE THE CAUSE
OF TOOTH HYPOPLASIA IN THE HUMAN.
Shaik PS, Pachava S; The Role of Vitamins and Trace Elements on Oral Health International Journal of Medical Reviews
(2017), page no 24

HYPERVITAMINOSIS A
• EXCESSIVE CONSUMPTION OF VITAMIN A LEADS TO
TOXICITY.
• THE SYMPTOMS OF HYPERVITAMINOSIS A INCLUDE
DERMATITIS
RAISED INTRACRANIAL TENSION
ENLARGEMENT OF LIVER,
SKELETAL DECALCIFICATION,
TENDERNESS OF LONG BONES,
LOSS OF WEIGHT,
IRRITABILITY,
LOSS OF HAIR,
JOINT PAINS
ELDERLY PEOPLE ARE MORE SUSCEPTIBLE TO VITAMIN A
TOXICITY

VITAMIN D
• VITAMIN D IS A FAT SOLUBLE VITAMIN.
• IT RESEMBLES STEROLS IN STRUCTURE
AND FUNCTIONS LIKE A HORMONE
• AVAILABLE IN TWO FORMS:
ERGOCALCIFEROL (VITAMIN D2)
FORMED FROM ERGOSTEROL-
PRESENT IN PLANTS
CHOLECALCIFEROL (VITAMIN D3)-
FOUND IN ANIMALS
• VITAMIN D IS REGARDED AS SUN-SHINE
VITAMIN.

DIETARY SOURCES
• FATTY FISH, FISH LIVER OILS, EGG YOLK
ETC.
• EXPOSURE OF SKIN TO SUNLIGHT FOR
SYNTHESISOF VITAMIN D;
• CONSUMPTION OF NATURAL FOODS;
• BY IRRADIATING FOODS (LIKE YEAST)
THAT CONTAIN PRECURSORS OF VITAMIN
D AND FORTIFICATION OF FOODS (MILK,
BUTTER ETC.).

RECOMMENDED DIETARY ALLOWANCE
• 400 IU OR 10 MG OF CHOLECALCIFEROL.
• IN COUNTRIES WITH GOOD SUNLIGHT
(LIKE INDIA) THE RDA FOR VITAMIN D IS
200 IU (OR 5 MG CHOLECALCIFEROL).

FUNCTIONS OF VITAMIN D
• CALCITRIOL (1,25-DHCC) IS THE BIOLOGICALLY ACTIVE
FORM OF VITAMIN D.
• IT REGULATES THE PLASMA LEVELS OF CALCIUM AND
PHOSPHATE.
• CALCITRIOL ACTS AT 3 DIFFERENT LEVELS
INTESTINE
KIDNEY
BONE

• ACTION OF CALCITRIOL ON THE INTESTINE
:
CALCITRIOL INCREASES THE INTESTINAL
ABSORPTION OF CALCIUM AND PHOSPHATE
• ACTION OF CALCITRIOL ON THE KIDNEY :
CALCITRIOL IS INVOLVED IN MINIMIZING THE
EXCRETION OF CALCIUM AND PHOSPHATE
THROUGH THE KIDNEY, BY DECREASING THEIR
EXCRETION ANDENHANCING REABSORPTION

ACTION OF CALCITRIOL ON THE BONE :
IN THE OSTEOBLASTS OF BONE, CALCITRIOL
STIMULATES CALCIUM UPTAKE FOR
DEPOSITION AS CALCIUM PHOSPHATE. THUS
CALCITRIOL IS ESSENTIAL FOR BONE
FORMATION.

VITAMIN D DEFICIENCY
• DEFICIENCY OF VITAMIN D CAUSES RICKETS
IN CHILDREN AND OSTEOMALACIA IN
ADULTS.
o RICKETS : DERIVED FROM AN OLD ENGLISH
WORD WRICKKEN; MEANING TO TWIST
• THERE IS INSUFFICIENT MINERALIZATION OF
BONE.
• BONES BECOME SOFT AND PLIABLE.
• THE BONE GROWTH IS MARKEDLY
AFFECTED.
.
vasudevan dm, sreekumari s, vaidyanathan k; textbook of biochemistry for dental students(2017)third edition, page no 140

• THE CLASSICAL FEATURES OF RICKETS ARE
BONE DEFORMITIES.
• WEIGHT-BEARING BONES ARE BENT
• CONTINUED ACTION OF MUSCLES ALSO
CAUSE BONE MALFORMATIONS.
• THE CLINICAL MANIFESTATIONS INCLUDE
BOW LEGS, KNOCK-KNEE, RICKETY
ROSARY, BOSSING OF FRONTAL BONES, AND
PIGEON CHEST

• OSTEOMALACIA: IS DERIVED FROM GREEK
(OSTEON-BONE; MALAKIA-SOFTNESS)
• THE BONES ARE SOFTENED DUE TO
INSUFFICIENT MINERALIZATION
• INCREASED OSTEOPOROSIS.
• LOWER SERUM CALCIUM, AND SERUM
PHOSPHATE LEVEL
• SERUM ALKALINE PHOSPHATASE IS
MARKEDLY INCREASED.

ORAL MANIFESTATIONS
• PROBLEM IN DENTIN AND PREDENTIN
CALCIFICATION
• MALFORMATION OF DENTIN.
• ESSENTIALAMOUNTS OF VITAMIN D
DURING THE DEVELOPMENT OF TEETH
HAS A RELATIONSHIP WITH DECREASED
FREQUENCY OF CARIES.
Shaik PS, Pachava S; The Role of Vitamins and Trace Elements on Oral Health, International Journal of Medical Reviews
(2017)

HYPERVITAMINOSIS D
• DEMINERALIZATION OF BONE (RESORPTION)
• INCREASED CALCIUM ABSORPTION FROM THE
INTESTINE, LEADING TO ELEVATED CALCIUM IN
PLASMA (HYPERCALCEMIA).
• PROLONGED HYPERCALCEMIA IS ASSOCIATED
WITH DEPOSITION OF CALCIUM IN MANY SOFT
TISSUES SUCH AS KIDNEYAND ARTERIES.
• FORMATION OF STONES IN KIDNEYS (RENAL
CALCULI).
• LOSS OF APPETITE, NAUSEA, INCREASED THIRST,
LOSS OF WEIGHT ETC.

VITAMIN E
• VITAMIN E (TOCOPHEROL) IS A
NATURALLY OCCURRING ANTIOXIDANT.
• ALSO CALLED ANTI-STERILITY
VITAMIN AS IT IS ESSENTIAL FOR
NORMAL REPRODUCTION.

DIETARY SOURCES
• MANY VEGETABLE OILS ARE RICH
SOURCES OF VITAMIN E.
WHEAT GERM OIL, COTTON SEED
OIL, PEANUT OIL, CORN OIL AND
SUNFLOWER OIL
• ALSO PRESENT IN MEAT, MILK, BUTTER
AND EGGS

RECOMMENDED DAILY ALLOWANCE
• INTAKE OF VITAMIN E IS DIRECTLY RELATED
TO THE CONSUMPTION OF
POLYUNSATURATED FATTY ACIDS (PUFA) i.e.,
REQUIREMENT INCREASES WITH INCREASED
INTAKE OF PUFA.
• A DAILY CONSUMPTION RECOMMENDED
10 MG (15 IU) FOR MAN
8 MG (12 IU) FOR WOMAN
• VITAMIN E SUPPLEMENTED DIET IS ADVISED
FOR PREGNANT AND LACTATING WOMEN

FUNCTIONS OF VITAMIN E
• MOST POWERFUL NATURAL ANTIOXIDANT-IT
INACTIVATES THE FREE RADICLES THAT ARE
CONTINUOUSLY GENERATED IN LIVING
SYSTEM
• PROTECTS RBC FROM HEMOLYSIS
• PREVENTS EARLY AGING.
• REDUCES THE RISK OF MYOCARDIAL
INFARCTION BY REDUCING OXIDATION OF
LDL
• IT PROTECTS THE POLYUNSATURATED FATTY
ACIDS (PUFA) FROM PEROXIDATION
REACTIONS.

VITAMIN E DEFICIENCY
• THE SYMPTOMS OF VITAMIN E DEFICIENCY
VARY FROM ONE ANIMAL SPECIES TO
ANOTHER.
• IN MANY ANIMALS, THE DEFICIENCY IS
ASSOCIATED WITH STERILITY, DEGENERATIVE
CHANGES IN MUSCLE, MEGALOBLASTIC
ANEMIAAND CHANGES IN CENTRAL NERVOUS
SYSTEM.
• IN HUMANS SEVERE SYMPTOMS ARE NOT
FOUND EXCEPT INCREASED FRAGILITY OF
ERYTHROCYTES AND MINOR NEUROLOGICAL
SYMPTOMS

ORAL MANIFESTATION
• PREMATURE ATROPHY AND PAPILLARY
LAYER EDEMA
• DEPIGMENTATION
• HYPOPLASIA
• UNNATURAL ERUPTION RATE
• PRODUCTION OF CYSTS
• FAT CELLS AND FIBROUS CONNECTIVE
TISSUE TAKE THE PLACE OF THE
PARENCHYMA OF THE SALIVARY
GLANDS
Shaik PS, Pachava S; The Role of Vitamins and Trace Elements on Oral Health, International Journal of Medical Reviews
(2017)

VITAMIN K
• VITAMIN K IS A FAT SOLUBLE
VITAMIN
• IT IS REQUIRED FOR THE
PRODUCTION OF BLOOD CLOTTING
FACTORS
• ESSENTIAL FOR COAGULATION (IN
GERMAN–KOAGULATION; HENCE THE
NAME K FOR THIS VITAMIN).

DIETARY SOURCES
• CABBAGE, CAULIFLOWER, TOMATOES,
ALFAALFA,
• SPINACH AND OTHER GREEN
VEGETABLES
• ALSO PRESENT IN EGG YOLK, MEAT,
LIVER,CHEESE AND DAIRY PRODUCTS

RECOMMENDED DAILY ALLOWANCE
• THERE IS NO RDA FOR VITAMIN K, SINCE IT
CAN BE ADEQUATELY SYNTHESIZED IN THE
GUT.
• IT IS HOWEVER, RECOMMENDED THAT HALF
OF THE BODY REQUIREMENT IS PROVIDED IN
THE DIET, WHILE THE OTHER HALF IS MET
FROM THE BACTERIAL SYNTHESIS.
• ACCORDINGLY, THE SUGGESTED RDA FOR AN
ADULT IS 70-140 MICROGRAMS/DAY.

FUNCTIONS OF VITAMIN K
• CONCERNED WITH BLOOD CLOTTING
PROCESS.
• BRINGS ABOUT THE POST-
TRANSLATIONAL MODIFICATION OF
CERTAIN BLOOD CLOTTING FACTORS.

VITAMIN K DEFICIENCY
• LEADS TO THE LACK OF ACTIVE
PROTHROMBIN IN THE CIRCULATION.
• BLOOD COAGULATION IS ADVERSELY
AFFECTED.
• THE INDIVIDUAL BLEEDS PROFUSELY EVEN
FOR MINOR INJURIES.
• THE BLOOD CLOTTING TIME IS INCREASED.

HYPERVITAMINOSIS K
ADMINISTRATION OF LARGE DOSES OF
VITAMIN K PRODUCES HEMOLYTIC
ANAEMIAAND JAUNDICE, PARTICULARLY
IN INFANTS.
THE TOXIC EFFECT IS DUE TO INCREASED
BREAKDOWN OF RBC

SUPPORTING STUDIES
VITAMIN K - ITS ESSENTIAL ROLE IN CRANIOFACIAL
DEVELOPMENT A REVIEW OF THE LITERATURE
REGARDING VITAMIN K AND CRANIOFACIAL
DEVELOPMENT.
• FIRST TRIMESTER DEFICIENCY RESULTS IN NEONATAL
MAXILLONASAL HYPOPLASIA OF VARYING DEGREES
• MATERNAL DIETARY DEFICIENCY OR USE OF NUMBER
OF THERAPEUTIC DRUGS DURING PREGNANCY, MAY
RESULT IN VITAMIN K DEFICIENCY IN THE EMBRYO
Howe AM, Webster WS; Vitamin K - its essential role in craniofacial development A review of the
literature regarding vitamin K and craniofacial development, Australian Dental Journal (1994)

WATER SOLUBLE VITAMINS
• THE WATER SOLUBLE VITAMINS ARE A
HETEROGENOUS GROUP OF COMPOUNDS
SINCE THEY DIFFER CHEMICALLY FROM EACH
OTHER.
• THE ONLY COMMON CHARACTER SHARED BY
THEM IS THEIR SOLUBILITY IN WATER.
• MOST OF THESE VITAMINS ARE READILY
EXCRETED IN URINE
• THEY ARE NOT TOXIC TO THE BODY
• THEY INCLUDE VITAMIN C AND B COMPLEX

VITAMIN C
• ALSO CALLED AS ASCORBIC ACID
• VITAMIN C IS A WATER SOLUBLE
VERSATILE VITAMIN.
• IT PLAYS AN IMPORTANT ROLE IN HUMAN
HEALTH AND DISEASE.

DIETARY SOURCES
• CITRUS FRUITS, GOOSEBERRY (AMLA),
GUAVA,
• GREEN VEGETABLES (CABBAGE,
SPINACH),
• TOMATOES, POTATOES (PARTICULARLY
SKIN)
• HIGH CONTENT OF VITAMIN C IS FOUND
IN ADRENAL GLAND AND GONADS.

RECOMMENDED DIETARY ALLOWANCE
• ABOUT 60-70 MG VITAMIN C INTAKE PER
DAY WILL MEET THE ADULT
REQUIREMENT.
• ADDITIONAL INTAKES (20-40%
INCREASE) ARE RECOMMENDED FOR
WOMEN DURING PREGNANCY AND
LACTATION

FUNCTIONS OF VITAMIN C
• COLLAGEN FORMATION: VITAMIN C PLAYS THE
ROLE OF A COENZYME IN HYDROXYLATION OF
PROLINE AND LYSINE WHILE PROTOCOLLAGEN IS
CONVERTED TO COLLAGEN
• BONE FORMATION : BONE TISSUES POSSESS AN
ORGANIC MATRIX, COLLAGEN AND THE
INORGANIC CALCIUM, PHOSPHATE ETC. VITAMIN
C IS REQUIRED FOR BONE FORMATION
• IRON METABOLISM: ASCORBIC ACID ENHANCES
THE IRON ABSORPTION FROM THE INTESTINE

• HEMOGLOBIN METABOLISM:
USEFUL FOR RE-CONVERSION OF
METHEMOGLOBIN TO HEMOGLOBIN
• ANTIOXIDANT PROPERTY: AS AN
ANTIOXIDANT, IT MAY PREVENT
CANCER FORMATION
• IMMUNOLOGICAL FUNCTION :
ENHANCES THE SYNTHESIS OF
IMMUNOGLOBULINS (ANTIBODIES)
• REDUCES THE RISK OF CATARACT
FORMATION

VITAMIN C DEFICIENCY
• SCURVY: CHARACTERIZED BY
SPONGY AND SORE GUMS, LOOSE
TEETH, ANEMIA, SWOLLEN JOINTS,
FRAGILE BLOOD VESSELS, DELAYED
WOUND HEALING HEAMORRHAGE,
OSTEOPOROSIS ETC.
• LACK OF VITAMIN C HALTS
OSTEOGENESIS AND PERIODONTAL
LIGAMENT ORGANIZATION

VITAMIN B COMPLEX
Disanto B; Guide to vitamins and minerals, vitamin b complex

CONCLUSION
• HORMONES AND VITAMINS PLAY A MAJOR ROLE IN
GROWTH AND DEVELOPMENT OF CRANIOFACIAL COMPLEX.
• QUANTITY OF VITAMINS CAN BE CONTROLLED THROUGH
DIET INTAKE AND THEREFORE SHOULD BE SUPPLEMENTED
IN APPROPRIATE PROPORTIONS DURING GROWTH AND
DEVELOPMENT.
• WHEREAS HORMONES, SINCE THEY ARE CONTROLLED BY
THE ENDOCRINE SYSTEM, IT IS IMPORTANT FOR US TO BE
ABLE TO IDENTIFYA POTENTIAL HORMONE DEFICIENCY
THROUGH THEIR VARIOUS CLINICAL MANIFESTATIONS AND
BE ABLE TO TREAT THE PARTICULAR PATIENT
APPROPRIATELY.

REFERENCES
• PREMKUMAR S; TEXTBOOK OF CRANIOFACIAL GROWTH(2012) 1ST
ED 46
• SEMBULINGAM K, SEMBULINGAM PREMA; ESSENTIALS OF
MEDICAL PHYSIOLOGY (2012),6TH ED P 372-426
• GRABER M, RAKOSI T, PETROVIC G; DENTOFACIAL ORTHOPEDICS
WITH FUNCTIONAL APPLIANCES(1985) P 12-30
• GUYTON AC, HALL JE; TEXTBOOK OF MEDICAL PHYSIOLOGY
(2011)12TH ED P 908-968
• GHOM A, GHOM S; TEXTBOOK OF ORAL RADIOLOGY,(2016),2ND ED
P 753-754
• SHAFER, HINE, LEVY; TEXTBOOK OF ORAL PATHOLOGY(2020) 9TH
ED P 2491-2508
• BURKHART NW, DELONG L; GENERAL AND ORAL PATHOLOGY FOR
DENTAL HYGIENIST,(2008)1ST ED 158-162

• SATYANARAYANA U,CHAKRAPANI U; BIOCHEMISTRY(2013),4TH ED
P 116-134
• VASUDEVAN DM, SREEKUMARI S, VAIDYANATHAN K; TEXTBOOK
OF BIOCHEMISTRY FOR DENTAL STUDENTS(2017)3RD ED P 140-141
• FUNATSU M , SATO K, MITANI H; EFFECTS OF GROWTH HORMONE
ON CRANIOFACIAL GROWTH. ANGLE ORTHOD:2006, VOL 76
• CANTU G, BUSCHANG H, GONZALEZ JL; DIFFERENTIAL GROWTH
AND MATURATION IN IDIOPATHIC GROWTH-HORMONE-DEFICIENT
CHILDREN, EUROPEAN JOURNAL OF ORTHOD (1997)
• RAMIREZ-YANEZ, SMID J, YOUNG WG, WATERS MJ;INFLUENCE OF
GROWTH HORMONE ON THE CRANIOFACIAL COMPLEX OF
TRANSGENIC MICE, EUROPEAN JOURNAL OF ORTHOD (2005)
• LEITCH V,BASSETT D,WILLIAMS G; ROLE OF THYROID HORMONES
IN CRANIOFACIAL DEVELOPMENT,2020

• DR. PRIYANKA PARIA, DR. RENUKA PATEL, DR. FALGUNI MEHTA;
ROLE OF NUTRITION AND HORMONE IN ORTHODONTICS (2020)V 7
• VERDONCK A, GAETHOFS M, CARELS C, ZEGHER F; EFFECT OF
LOW-DOSE TESTOSTERONE TREATMENT ON CRANIOFACIAL
GROWTH IN BOYS WITH DELAYED PUBERTY, EUROPEAN JOURNAL
OF ORTHOD (1999)
• SHAIK PS, PACHAVA S; THE ROLE OF VITAMINS AND TRACE
ELEMENTS ON ORAL HEALTH INTERNATIONAL JOURNAL OF
MEDICAL REVIEWS (2017)
• HOWE AM, WEBSTER WS; VITAMIN K - ITS ESSENTIAL ROLE IN
CRANIOFACIAL DEVELOPMENT A REVIEW OF THE LITERATURE
REGARDING VITAMIN K AND CRANIOFACIAL DEVELOPMENT,
AUSTRALIAN DENTAL JOURNAL (1994)

role of harmones and vitamins in craniofacial growth and development

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