AVITAMINOSIS FAT

SOLUBLE VITAMINS

 A fat soluble vitamin.

CHEMISTRY
Vitamin D is a sterol, it contains steroid nucleus

(Cyclopentanoperhydrophenanthrene ring)
Vitamin D function like a hormone
Also referred to as antirachtic vitamin.
Forms of vitamins
Vitamin D2 (ergocalciferol)
Vitamin D3 (Cholecalciferol)

CH3

Ergocalciferol and Cholecalciferol are sources for

vitamin D activity and are referred as provitamins

Active form: the active form of vitamin D is

1,25 Dihydroxycholecalciferol and is also

called as calcitriol.
Both hydroxylase enzymes (of liver and

kidney) require cytochrome P450, NADPH

and molecular oxygen for hydroxylation
process

Storage
25 hydroxycholecalciferol is the major

storage and circulatory form of vitamin D

CALCIUM PHOSPHOROUS
HOMEOSTASIS

DAILY REQUIREMENTS

Children - 10 gm/day or 400 IU/day

Adults

- 5 gm/day

or 200 IU/day

Pregnency,lactation -10 gm/day or 400 IU/day

Above the age of 60 yrs

- 600 IU /day

Sources of vitamin D:
Exposure to sunlight produces cholecalciferol
Good sources includes fatty fish, fish liver

oils, egg yolk etc

Milk is a good source

Deficiency of vitamin D causes rickets in

children and osteomalacia in adults

Rickets:
It is a vitamin D deficiency state in children
Causes: Dietary deficiency and non-

exposure to sunlight.

CLINICAL FEATURES

ORAL
MANIFESTATIONS
Developmental abnormailities of

dentin and enamel

Delayed eruption
Misalignment of teeth
High caries index
Enamel hypoplasia
Eruption rate is retarded of both
deciduous and permanent teeth

Biochemical findings:

Decreased serum calcium (9-11mg/dl)

Decreased plasma phosphorous (3-

4.5 mg/dl)
Increased plasma alkaline

phosphatase (30-130 IU)

Also known as adult rickets

Bones affected flat bones and diaphyses

of long bones
Etiology:
Inadequate exposure to sunlight
Low dietary intake
Malabsorption

RADIOGRAPHIC FEATURES
Asymmetric deformities of stress bearing bones.
Longitudinal hairline fractures.

Clinical Features:
Female more affected than male
Remodelling of bones in absence of adequate
calcium.
Bowing of long bones may occur due to weight
of the body
Flattening of pelvis bones may cause difficulty
during labour
ORAL MANIFESTATIONS
Periodontitis reported in women suffering from
osteomalacia

HISTOLOGY
1. Bone remodelling with inadeqaute calcification
2. Cortical bone thin.

TREATMENT AND PROGNOSIS

1. Diet enriched in Vitamin D (Milk)
2. Hormonal therapy and flouride.

Also known as Renal Osteodystrophy

In chronic renal failure, 1 hydroxylase

activity is decreased leading to decreased

synthesis of 1,25 DHCC
Painful crippling disease.
TREATMENT AND PROGNOSIS
Condition is treated by giving 1,25 DHCC

preparations
But prognosis depends on the treatment of

underlying renal disease.

VITAMIN D RESISTANT
RICKETS
(FAMILIAL HYPOPHOSPHATSIA,
REFRACTORY RICKETS, PHOSPHATE
DIABETES)
CHARACTERISED BY:
1. Hypophostameia, hypophosphaturia
2. Familial ( x linked dominant)
3. No response to vitamin D usual doses
4. Decreased Ca and P absorption
5. Dwarfism

CLINICAL FEATURES
Dwarfism
Bowing of legs
Pseudofractures
Skull and sitting deformities
Muscular weakness and atony
may occur

ORAL MANIFESTATIONS
Formation of globular, hypocalcified dentin
Clefts in pulp horn region
Wide root canal and pulp chambers
Pulp horns elongated and extending neat DEJ.
Lamina dura absent
Alveolar bone abnormal

High pulp horns and large pulp

chambers are common in patients
with x-linked hypophosphatemic
dominant rickets

HISTOLOGICAL FEATURES
Cartilage plate and shaft of long

bones altered
Failure of bone salt deposition
Rachitic metaphysis- Broad zone
between cartilage cells and shaft.

TREATMENT AND
PROGNOSIS
1. High Doses of vitamin D
(50,000 100,000 IU)
2. 25- hydroxycholecalciferol in
lower doses more successful
(10,000 25,000 IU) in
combination with oral phosphate
administration.

HYPOPHOSPHATASIA
Autosomal recessive disorder
Deficiency of alkaine phosphatase
Excretion of phosphoethanolamine in urine

CLINICAL FEATURES
BASED ON CLINICAL FEAUTURES, It is of

three clinical forms

1. INFANTILE severe rickets, hypercalcemia
and death
2. CHILDHOOD increased infection, growth
retardation, rachitic rosary. Pulmonary, GI
tract and renal disorders also present
3. ADULT spontaneous feactures

ORAL MANIFESTATIONS
Loosening and premature loss of teeth

mainly incisors.
Gingivitis

RADIOGRAPHIC FEATURES

Metaphyses are spotty, streaky or irregular

ossification
Hyplocalcification of tooth, presence of large
pulp chambers.
Alveolar bone loss

HISTOLOGY
Increase width of cartilage with widening

of hypertrophic cell zone

Penetration of cartilage by marrow
Large amount of inadequately calcified
osteoid .
Absence of cementum or some poorly
formed cementum.

TREATMENT
Partial improvement by high doses of

vitamin D
Moderate improvement by oral dosinf of
phosphate
Prognosis not good.

PSEUDOHYPOPHOSPHATA
SIA
Similar to hypophosphatasia but with normal

serum alkaline phosphatase

Osteopathy of long bones and skull
Exfoliation of decidous teeth
Hypercalcemia
Phosphoethanolaminuria

 Vitamin D is stored mainly in liver

Vitamin D is most toxic in overdoses
Toxic effects include demineralization of bones and

increased calcium absorption from intestine, leading

increased plasma calcium (hypercalcemia)
Hypercalcemia is associated with deposition of

calcium in many soft tissues such as kidney and

arteries
It leads to formation of stones (renal calculi)
High consumption is associated with loss of

appetite, nausea, increased thirst, loss of weight etc

Calcitriol is considered as an important

calciotropic hormone, while cholecalciferol

is the prohormone
1. Vitamin D3 (cholecalciferol) is synthesized
in the skin by the UV rays of sunlight
2. The biologically active form of vitamin D,
calcitriol is produced in the kidney
3. Calcitriol has target organs-intestine, bone
and kidney

4. Calcitriol action is similar to that of steroid

hormones
It binds to a receptor in the cytosol and the
complex acts on DNA to stimulate the
synthesis of calcium binding protein
5. Calcitriol synthesis is self-regulated by a
feedback mechanism i.e., calcitriol
decreases its own synthesis
6. Actinomycin D inhibits the action of calcitriol,
calcitriol exerts its effect on DNA leading to
the synthesis of RNA (transcription)