AVITAMINOSIS – FAT SOLUBLE

VITAMINS

A fat soluble vitamin.

CHEMISTRYVitamin – 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

Storage25 – 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 eruptionMisalignment of teethHigh caries indexEnamel hypoplasiaEruption 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 maleRemodelling of bones in absence of adequate calcium. Bowing of long bones may occur due to weight of the bodyFlattening of pelvis bones may cause difficulty during labour

ORAL MANIFESTATIONSPeriodontitis reported in women suffering from osteomalacia

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

TREATMENT AND PROGNOSIS

HISTOLOGY1. Bone remodelling with inadeqaute calcification

2. Cortical bone thin.

Also known as Renal OsteodystrophyIn chronic renal failure, 1 α – hydroxylase

activity is decreased leading to decreased synthesis of 1,25 – DHCC

Painful crippling disease.TREATMENT AND PROGNOSISCondition is treated by giving 1,25 –

DHCC preparationsBut 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 doses4. Decreased Ca and P absorption5. Dwarfism

CLINICAL FEATURES

DwarfismBowing of legsPseudofracturesSkull and sitting deformitiesMuscular weakness and atony may occur

ORAL MANIFESTATIONS

Formation of globular, hypocalcified dentinClefts in pulp horn regionWide root canal and pulp chambersPulp horns elongated and extending neat DEJ.Lamina dura absentAlveolar 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 depositionRachitic 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.

HYPOPHOSPHATASIAAutosomal recessive disorderDeficiency of alkaine phosphataseExcretion 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 MANIFESTATIONSLoosening 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

HISTOLOGYIncrease width of cartilage with widening

of hypertrophic cell zonePenetration of cartilage by marrowLarge 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.

PSEUDOHYPOPHOSPHATASIA

Similar to hypophosphatasia but with normal serum alkaline phosphatase

Osteopathy of long bones and skullExfoliation of decidous teethHypercalcemiaPhosphoethanolaminuria

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)