CALCIUM AND PHOSPHOROUS METABOLISM

CALCIUM:
1) Introduction
2) Sources
3) Daily Requirements
4) Distribution of Ca+2 in the body
5) Function of Ca+2
PHOSPHOROUS
1) Sources
2) Daily Requirements
3) Distribution
4) Function of PO4-3
5) Concept of Ca+2 and PO4-3 balance.
6) Absorption of Ca+2 and PO4-3
7) Factors controlling the absorption of Ca+2 and PO4-3
8) Hormonal control of Ca+2 metabolism
a. Vit O3
b. PTH
c. Calcitonin
9) Other hormones effecting Ca+2 metabolism
10)Excretion of calcium and PO4-3
11)Clinical importance
12)Conclusion
13)References

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INTRODUCTION

As dentist it is vital for us to have a complete understanding of the general

metabolism of Ca+2 and phosphorous as it is these minerals that help in the

formation and the maintenance of the teeth and their supporting bony structure 2

points need to be kept in mind during the course of this discussion.

1) Ca+2 metabolism is a very complicated and controversial topic, on which no

definite conclusion has yet been reached, which is acceptable by all

researchers.

2) This topic deals with factors affecting Ca +2 metabolism in the body as a

whole and it should not be assumed that an these factors necessarily affect

the teeth.

Distribution of Calcium in the body:

Total body calcium  1100-1200gms i.e. 1.5% of body weight.

Of this about 99% of the Ca+2 in the body is in crystalline form within the

skeleton and teeth, of the remaining 1% about 0.9% is found intracellularly within

the soft tissues.

< 0.1% is present in the ECF.

Normal serum plasma Ca+2 levels = 10.0 – 10.5mg/100ml.

Approximately half of the plasma Ca+2 either bound to plasma proteins (or)

complexed with PO4-3, citrates, other half of the plasma Ca +2 is freely diffusible

Ca+2.

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Diffusable Ca+2

(or) Ionized Ca+2 – 5.0mg/dl

- Free Ca+2 salts.
- Readily pass into interstitial fluid and interact with the cells.
- Biologically active.
- Constitutes < one thousandth of the total Ca+2 in the body.
- Plays a vital role in number of essential activities.
e.g.
1. Neuromuscular excitability.
2. Excitation – contraction coupling in cardiac and smooth
muscle.
3. Maintenance of tight jun’ between cells.
4. Clotting of blood.

Non diffusible Ca+2 (4.5mg/dl):

Combined with plasma proteins.

i.e. mainly
Albumin 4.0mg/dl
Globulin 0.5mg/dl
Non ionized Ca+2
Combined with PO4-3, CO3-, citrates.
Biologically inactive.
Not available freely 0.5mg/dl.

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Daily Requirements of Calcium:

The daily requirement of Ca+2 is about 300mg but intake should be more because

only is absorbed. So the dietary intake of Ca+2 is 60% around 1.0gm/day.

- The recommended dietary allowance for Ca+2 is 0.5-0.8g/day.

- Low Ca+2 intake will absorb a high % this believed to be due to saturation

of cells active transport mechanism rises.

- In pregnancy RDA is 1.5g/day. During lactation, Ca +2, is secreted into the

milk for the infant, RDA is 2.0g/day.

- WHO estimate of Ca+2 – 360mg for newborn infants.

800 for children
1200mg for pregnant, adolescents and lactating
women.

Source:

The source of Ca+2 are mainly milk and milk products and cheese etc

The other sources are Eggs, Fish, meat, leafy vegetables.

Vegetables:
Cauliflower
Fruits – Orange,
Beans
Bread (if fortified)
Hard water etc.
Nuts – Almond, peanuts chick pees
Milk Ca+2 is absorbed better because organic salts of Ca+2.

Functions of Ca+2:

1) Contributes to hardness of bone and is a major component of teeth.

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2) Stabilizing cell membrane + permeability.

Increased blood Ca+2 – Decreased permeability

Decreased blood Ca+2 – Increased permeability.

3) Teeth are made of Ca+2 PO4- are essential for processing of food.

4) Retention of teeth in the socket depends on the anchorage of PDL in

calcified bone cementum.

5) Maintenance of excitability of nerve and muscle.

6) Normal skeletal and cardiac muscle contraction.

7) Neurotransmitter release.

8) Synthesis of nucleic acids and proteins.

9) Maintenance of tight junctions between cells.

10)Clotting of blood: Ca+2 serves as a cofactor in several steps of the cascade

of reactions that lead to clot formation.

11)Production of milk.

12)Activation of enzymes e.g. ATP ase succinate dehydrogenase lipase.

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PHOSPHOROUS

Occur as phosphate ion PO4-3. Most of the PO4-3 is intimately associated with Ca+2

in the metabolism of bones and teeth. In light of current knowledge, PO 4-3

concerned in more vital processes than is Ca+2.

Distribution of phosphorous in the body:

Human body contains 500-800mg of phosphate which is 85% in the bone.

15% in the liver, pancreas and brain.

Daily requirements of PO4-3 ranges from:

240mg  Infants.

800mg  Adult.

1200mg  Pregnant, lactating woman and adolescents.

Normal serum PO4- levels are

2.5 to 4.5mg/100ml

Serum inorganic form Serum organic form

3-4 mg/100ml in adults Remaining in form of

5-6mg/100ml in children phospholipids, glycerophosphates.

Inorganic PO4-3 is incorporated into

hydroxyapatite which gives rigidity
to bone and teeth

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Sources:
Same as calcium.
Specially cereals and pulses.
In hard water No. PO4-3.

Absorption:
70% ingested PO4-3 is absorbed from alimentary tract.
30% is exerted in the faeces.
Absorption depends upon presence of Ca+2 and Na+2 ions and vitamin D meta.

Absorption enhanced by:

1) Low Ca+2 diet.
2) Growth hormone.
3) PTH.
4) Vitamin D.
5) Acids.

Absorption decreased by:

1. High Ca+2 diet.
2. Vit. D deficiency.
3. Antacid – Aluminium hydroxide.

Excretion :
Daily intake of 900mg of inorganic PO4-3.

Urinary output to 600mg

In kidney  PO4-3 undergoes glomerular filtration.


Reabsorption in the proximal tubule and distal tubule.

Decreased in Increased in

1) Low – PO4-3 diet. 1) High PO4-3 diet.

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 2) C.H. 2) Vit.D excess
3) Hypoparathyroidism 3) Hypoparathyroidism.

Functions of Phosphorous:

1) Formation of bone and teeth and essential constituent of all cells.

(Nucleoproteins, nucleus, phospholipids).

2) They provide energy rich bonds in compounds like adenosin triphosphate

which is important for muscle contraction.

3) Help in regulation of pH of blood and urine. Urinary buffer, which

regulates urinary pH, cell + blood pH (Acid + alkaline phosphate buffer

system).

4) PO4- forms an intermediate stage in metabolism of fat and carbohydrate.

5) They form part of co-enzyme or pyridoxal phosphate which is necessary in

decarboxylation and transamination of certain aminoacid.

6) PO4-3 forms a part of organic molecules as the nucleic acids (DNA and

RNA).

Concept of Calcium Balance:

This term is used to describe the amount of Ca +2 either stored (or) lost by the body

over a specific period of time. This can be calculated by deducting the amount of

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Ca+2 in the urine and foeces from the calcium taken in from the diet. Ca +2 in diet –

Ca+2 in faeces absorbed – Ca+ urine. Ca+2 host gained.

E.g.

- If 1.0gm Ca+2 in diet – 0.7g in faeces – 0.3 absorbed. 0.1 griet gain -

- 0.3urine.

- The Ca+2 balance values are said to change with age.

- In a growing child there is a net gain for growing and mineralizing

skeleton.

- In an aging adult there is a net loss as Ca+2 from bone is lost due to

conditions like osteopororis. Hence amount of Ca +2 lost is greater

than Ca+2 intake.

Absorption of Calcium Phosphorous:

It is seen that almost all the food taken in through the diet i.e. almost completely

absorbed in the gut where as the amount of minerals absorbed is very negligible.

This could be due to the various factors affecting the absorption of Ca+2 and PO4-.

The factors can be studied under:

1) Factors affecting mucosal cells.

2) Factors influencing Ca+2 absorption in the gut.

1) Factors affecting mucosal cells:

a. Vitamin D and Ca+2 absorption.

b. Effect of dietary Ca+2 intake and Ca+2 need.

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 c. Effect of pregnancy and growth.

d. Parathyroid hormone.

Vit. D and Ca+2 absorption:

The active form of vit D (or) 1,25 DHCC increases the absorption of Ca +2 in the

gut, kidney and bone. This absorption of Ca+2 is directly related to the increased

concentration of calcium binding protein produced by increasing synthesis of

mRNA.
1-25 DHCC.

Increases synthesis of mRNA.

Increases level of CBP.

Increases Ca plasma level.

Effect of Dietary Ca+2 intake of Ca+2 need:

It is seen by means of experiments that the amount of Ca +2 stored in the body is a

factor which influences Ca+2 absorption.

This factor can be better understood by means of an example.

Rottensten in 1938 used 2 groups of rats for his experiment.

He fed : 1st group and 2nd group
0.15% calcium   0.8% Ca+2
4 weeks 4 weeks

4 weeks later he observed that:

Calcium stored 190mg  570 mg Ca+2 stored thus suggesting that greater the

dietary intake of Ca+2 greater amount of Ca+2 stored.

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In the 2nd stage of experiment both groups received 0.4% Ca+2 for 5 weeks.

0.4% Ca+2 0.4% Ca+2

5 weeks 5 weeks

5 weeks later

absorbed 900mg 600mg

amount

This suggested that the group with a low Ca+2 store absorbed more than that the

group with a high Ca+2 store. Thus suggesting that that the amount of Ca+2

absorbed is directly dependent on the amount of Ca +2 present in the store. This

kind of adaptation mechanism is directly under the control of formation of 1) 25

DHCC.

Effect of Pregnancy and Growth:

Pregnancy:

During pregnancy the amount of dietary Ca +2 absorbed increases especially in the

later months of pregnancy. Half of the Ca+2 absorbed during pregnancy goes to the

developing foetus and the remaining half is stored in the mother’s skeleton as a

reserve for lactation.

2 hormones are active during pregnancy.

1) Placental lactogen – increases Ca+2 absorption.

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 2) Oestrogen – Acts by increasing release of PTH which increases Ca +2

absorption indirectly. Hence in later stages of pregnancy Increased PTH

levels reported.

Growth :

During growth period of children the growth hormone levels are high. This GH

acts by increasing Ca+2 absorption and reducing amount of endogenous Ca +2

excretion.

Parathyroid Hormone:

Parathyroid hormone is one of the main hormones controlling Ca +2 absorption. It

mainly acts by controlling the formation of 1,25 DHCC which is active form of

Vit. D which is responsible for increased Ca+2 absorption.

Calcium phosphorous Ratio:

An increase in the plasma calcium level causes a corresponding decrease in

absorption of PO4- and vice versa. The product of Ca +2 and inorganic phosphate

of the blood is always constant (Ratio 2 Ca: 1P).

After parathyroidectomy plasma Ca+2 falls and PO4-3 rises, where as the opposite

happens after administration of PTH. However in rickets the absorption of Ca +2

and PO4- deficient, both Ca+2 and PO4-levels are reduced.

Factors influencing availability of Ca+2 in the gut:

1) pH of intestine.

2) Amount of dietary Ca+2 and phosphorous,

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3) Phytic acid and phytates.

4) Effect of oxalates.

5) Effect of fat.

6) Effect of proteins and aminoacids.

7) Effect of carbohydrates.

8) Bile salts.

1) pH of intestine:

It is seen that the acid of the gastric juices dissolves most of the calcium salts

and inorganic phosphates in the diet hence allowing greater amount of Ca +2

available for absorption.

In the lower part of small intestine the pH is said to be more alkaline thus

causing Ca+2 salts to undergo precipitation. Hence Ca +2 absorption occurs only

in the upper part of small intestine where the pH is acidic.

In patients with achlorhydria/gastrectomy less Ca+2 absorption takes place.

2) Amount of dietary Ca+2 + PO4-3.

The levels of dietary Ca+2 and phosphorous is increased the amount of Ca +2

and PO4- absorbed also increased but only upto a certain limit beyond which

no more absorption takes place. This is because the active transport system in

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the mucosal cells can deal with only a certain load of calcium, once this load is

exceeded the remaining calcium either is excreted on passively diffuses in the

lower parts of the gut. This is a homeostatic mechanism for preventing

excessive concentration of Ca+2 in the blood (or) tissues, which could have a

hazardous effect.

3) Phytic acid and phytates:

Phytic acid and phytates are found in foods like oatmeat, whole meat and

cereals. They are considered to be anti-calcifying factors as they combine with

the Ca+2 of the diet thereby forming insoluble salts of Ca +2, which are not

absorbable.

Hence if these phytates are taken in a diet where the Ca +2 intake is low (or)

Vitamin D intake is low it is seen that severity of the deficiency diseased

worsens. The effect of phytates is said to be quantitative and can be

neutralized by adding sufficient extra Ca+2 to the diet.

The homeostatic regulation of Ca+2 ion concentration:

The homeostatic regulation of Ca+2 ion concentration involves simultaneous

adjustments in the rates of Ca+2 ion uptake, storage and loss. Two antagonist

hormones perform the necessary adjustments; calcitonin, released when Ca +2

ion can become abnormally high, and parathormone, related when Ca +2 ion

conc. are abnormally low. Together they maintain Ca +2 ion conc. within

homeostatic limits.

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 Decreased intestinal
absorption of
calcium

Increased Thyroid gland Ca+2

Increased excretion
Ca+2 produces levels
of Ca+2 in kidneys
levels Calcitonin decline

Ca+2 deposition in
bone

Homeostasis;
Homeostasis disturbed Normal Ca+2 levels Homeostasis
restored
8.5 to 11mg%

Increased Ca+2
absorption from
intestine

Decreased Parathyroid
Release of stored Increased
Ca+2 gland secretes
Ca+2 from bone Ca+2 levels
levels parathormone

Enhanced
reabsorption of Ca+2
in kidneys

Ca+2 Homeostasis:

Involves the immediate adjustments required to maintain a constant free

plasma Ca+2 conc. on a minute to minute basis.

This depends largely on rapid exchange between the bone and ECF lesser

extent by modifications in urinary excretion of Ca+2.

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 2nd: Ca+2 balances: Involves the more slowly responding adjustment in

intestinal Ca+2 absorption as well as adjustments in urinary Ca +2 excretion

required to maintain a constant total amount of Ca+2, in the body.

Control of Ca+2 balance ensures that Ca+2 intake is equivalent to Ca+2 excretion

over the long term (weeks to months).

Effect of Oxalates:

Oxalate is another substance present in certain foods like spinach and rhubarb

leaves. These oxalate precipitate significant amount of Ca +2 from the diet (or)

from the digestive juices thereby decreasing amount of Ca +2 available for

absorption. Hence it is noticed that after eating rhubarb leaves certain roughness

can be experienced on the surface of the teeth which is due to the precipitation

and deposition of Ca+2 oxalate crystals (Ca+2 from saliva) on the teeth.

Effect of Fat:

Fat combined with Ca+2 forming insoluble Ca+2 soaps, which decrease Ca+2

absorption but increase in the availability of PO4-3 for absorption.

Effect of proteins and aminoacids:

Considerable increase in Ca+2 absorption occurs with a high protein diet.

Proteins and aminoacids effects Ca+2 in 2 ways:

1) Protein form soluble complexes with Ca+2 thus allowing Ca+2 to remain in a

form that is easily absorbable.

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Protein metabolisms lead to formation of certain acids that encourages the

removal of Ca+2 from the skeleton. Hence urinary Ca+2 level also increases with a

richer protein diet. (Overall Ca+2 loss may be seen).

Hence a high protein diet is a possible factor for osteoporosis.

Fats combine with Ca+2 that urinates phosphorus for absorption. Hence excess fats

under Ca+2 absorption favours PO4-3 absorption. But under such conditions the

increased absorption is of no value, as this absorbed PO 4-3 cannot be retained

without calcium because of this excess PO4-3 is quickly excreted.

Effect of carbohydrates:

Certain carbohydrates like lactose create an acidic pH in the gut by favoring

growth of acid producing organisms. This acidic environment of gut favors Ca +2

absorption. Contradictory studies shows that an increased level of Ca +2 is seen in

the body but not by increase in Ca+2 absorbed but by decrease in Ca+2 excreted in

urine.

Bile salts:

Bile salts favors Ca+2 and PO4-3 absorption as it dissolves fats thereby allowing >

amount of Ca+2 and PO4-3 to be available for absorption.

Factors favouring Ca+2 absorption:

2) Parathyroid hormone.

3) High protein diet with amino acids  lysine arginine.

4) Vit. D.

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 5) Negative Ca+2 balance.

6) Acidic residues in intestine or acidic pH.

7) Bile salts – By their hydrophobic action on Ca+2 soaps.

8) Pregnancy, lactation, growth.

9) Lactose, sex hormones.

Factors inhibiting Ca+2 absorption:

1) Oxalates, phytates, phytic acid

2) Excess PO4-3.

3) Excess intestinal lipids.

4) Corticosteroid, thyroid hormones.

5) Less acidic pH.

6) High body stores of Ca+2.

Calcitonin:

Calcitonin is secreted by the parafollicular (or) C-cells of thyroid gland. Hence

the name thyrocalcitonin. Acts to maintain the integrity of bone.

Regulation of Secretio of Calcitonin:

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The release of calcitonin is regulated by the plasma calcium levels. A rise in the

plasma calcium level above 10mg% stimulates the release of calcitonin.

Hence, plasma Ca levels controls the direction of PTH and calcitonin. In adults,

role of calcitonin is very minor and normal Ca level is maintained by PTH.

Calcitonin plays a major role in pregnancy (or) it protects the bones of the mother

from excessive loss of Ca as during pregnancy PTH and 1,25 DHCC levels are

high.

Decreased Plasma Ca+2 Increased Plasma Ca+2

Parathyroid glands Thyroid cells

Increased PTH Increased Calcitonin

Increased Plasma Ca+2 Decreased plasma Ca+2

Negative feedback loops controlling parathyroid hormone and calcitonin

secretion.

Actions:

Calcitonin has two effects on bone:

1st  (short term basis) calcitonin decreases Ca +2 movement from the bone fluid

into the plasma.

2nd  (long term basis) Calcitonin decreases bone resorption by inhibiting the

activity of osteoclasts. The suppression of bone resorption result in decreased

plasma PO4-3 levels. (Hypophosphatemia).

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Decreased plasma Ca+2 conc. (Hypocalcemia).

1st action: The major actions of calcitonin administration is a rapid fall in the

plasma calcium concentration, caused by inhibition of bone resorption.

Clinical Applications:

1) Calcitonin is useful in treatment of hypercalcemia due to parathyroid

adenoma and vit. D intoxication.

2) Useful in the treatment of Paget’s disease in whom overgrowth of bone

leads to skeletal deformity and pain. Calcitonin administration relieves

pain, restores normal bone structure.

2nd action:

It increases urinary excretion of Ca by inhibiting reabsorption in distal convulted

tubule. Decreased Ca+2 absorption in intestine.

3rd – Has protective influence on bone or its, foetus and growing children.

4th: Protects maternal bone during pregnancy.

It is released by many GIT hormones like:

- Gastrin.

- Cholecystokinin.

- Secretin.

- Glycagon.

- The blood conc. of calcitonin is more in males than females. So

susceptibility for osteoporosis is more in female.

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Other hormones affect Ca+2 metabolism:

1) Grown hormone:

- Increase absorption of Ca+2 in small intestine and also increase

excretion in urine   total body Ca+2.

- Stimulates protein synthesis in bone by production of IL- GF Inter

leukin growth factor.

- Stimulates in length of long bones by stomatomedin which acting on

cartilage during growth.

- In acromegaly  growth hormone leads to thickening and

lengthening of bones.

2) Insulin: Favours bone formation and important in bone growth during

foetal and childhood development.

3) Testosterone and others:

- Act on cartilage and results in increased growth of secondary sexual

characteristics of bones like fused growth of shoulders, more

developed supraorbital ridges and greater mandibular growth in

males.

4) Oestrogen:

- Acts on cartilage and converts into bone.

- Promotes growth to increase size of pelvic bone. So shoulder to hip

width more in males than female.

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 - Osteoporosis in post-menopausal women.

5) Prolactin:

 Stimulates both intestinal absorption and Ca +2 mobilization from

bone and by favouring hydroxylation of vit. D.

6) Thyroid hormone (T3 and T4):

- Stimulates bone growth (so dwarfism in hypothyroidism).

- In adults hypercalcaemia and hypercalciuria leading to osteoporosis.

7) Steroids:

- Anti Vit.-D action, by  absorption of Ca in small intestine and 

renal excretion of Ca.

- Inhibit osteoclast formation and  activity of osteoclasts present 

 Ca level in plasma. Long term steroid therapy leads to

osteoporosis.

Excretion of Calcium and Phosphorous:

Ca is said to be excreted both in the faeces and in the urine. About 90% of the

total amount of Ca is secreted in the faeces.

Ca of the urine is excreted as (CaCl2) calcium chloride and (CaPO4)  10%

remaining.

The approximate daily turnover rates of Ca in an adult are as follows:

Intake 1000mg.

Intestinal absorption 350mg

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Secretion in GI juice 250mg

Net absorption over secretion 100mg

Loss in the faeces 200mg

Excretion in the urine 100mg

Phosphorous is excreted primarily through the urine. Almost 2/3 rd of total

phosphorous that is excreted is found in the urine as phosphate of various cations

phosphorous found in the faeces is the non-absorbed form of phosphorous.

Buffer action of phosphorous in blood:

Two varieties of phosphates are present in the blood.

Alkaline Acidic

H2PO4 HPO4

Concentration is about 1.05m mol/lit 0.26mmol/lit.

In the plasma they are in a ratio of alkaline 4:1 acidic.

Where pH of extra-cellular fluid becomes more acidic there is a relative increase

in H2PO4- and HPO4- and the opposite happen when fluid is alkaline. The average

total quantity of inorganic phosphorous ranges between normal limits of 3-4mg/dl

in adults and 4-5mg/dl in children.

Clinical significance:

 Ca (serum)  Ca (serum)

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 1) Hyperparathyroidism.
2) Hypervitaminosis (Vit. D).
3) Multiple myeloma.
4) Sarcoidosis.
5) Thyrotoxicosis.
6) Milk alkali syndrome.
7) Infantile hypercalcemia
1) Renal failure.
2) Hypoparathyroidism.
3) Vit. D deficiency.
4) Tetany.
5) Malabsorption syndrome.
6) Long term steroid therapy.

Impairments in blood calcium:

1) Hyper calcaemia: Increased level of Ca2 in the blood.

Symptoms:

- Tiredness.

- Loss of appetite.

- Nausea.

- Vomiting.

- Constipation.

- Polyuria.

- Dehydration.

- Loss of muscle tone.

- Decreased excitability of muscles and nerves.

Conditions in which it occurs:

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 - Hyperparathyroidism.

- Acute osteoporosis.

- Vit. D intoxication.

- Thyrotoxicosis.

Pathologic Calcifications of soft tissues:

3 theories have been forwarded for the mechanism of calcification.

a) Nucleation theory:

Ca+2 is deposited both inside and outside the cells (in mitochondria) which later

coalesce together to form calcified tissues.

This proposes that organic m4 components facilitate precipitation by acting us

heterogenous nucleating agents like collagen, phospholipids which act on specific

phosphorylating sites.

b) Booster theory: This theory proposes the existence of a mechanism

to boost the local Ca and PO4-3 ion product to a point where precipitation

occurs.

c) Matrix vesicles:

Small round vesicular extracellular mx vesicles about 100nm in diameter are

involved in the initiation of calcification. They are probably arrived from

leuprocesses originating from the plasma membrane.

(i) Dystrophic calcification:

- Precipitation of Ca in degenerating and dead tissue occur.

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 - Common sites are – blood vessels, Kidney.

(ii) Metastatic calcification:

- Due to excess Ca in the circulating blood, they are deposited in

previously undamaged tissue.

Usually occur in:

1. Hypervitaminosis D.

2. Hyper parathyroidism.

3. Destructive lesions of the bones.

- Common sites are – Blood vessel, Kidney.

(iii) Calcinosis:

Is calcification occurring in / under skin and can be associated with scleroderma.

Dental findings:

Ricketts:

- Development of abnormality in enamel and dentin.

- Delayed eruption of teeth.

- Malalignment of teeth.

- Higher caries index.

- Wider predentine zone.

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 - Increased amount of interglobular dentine.

Treatment:

Supplying adequate amount of Ca and phosphate in diet and administration of

large amounts of Vit. D.

Osteomalacia:

Severe periodontitis.

Vit. D. Deficiency:

Ricketts Osteomalacia

- Occur in children. - Occur in adults.

- Mainly affects the long bones - Mainly affects the flat bones

in body and ribs. in the body.

- Occurs due to failure in - Especially seen in post and

mineralization, due to lack of Ca menopausal women who have a

level, the cartilaginous form of decreased dietary Ca intake and

bone is said to persist. decreased exposure to the sun

- The cartilage continuous to resulting in increased removal

grow and proliferate thus of Ca from the bone causing

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 resulting in localized areas of softening of the skeleton and its

cartilage proliferation. (Rickets distortion.

rosary, beaded bone formation).

- The weight of the body on

the uncalcified long bones result

in the bowing of legs (knock

kness).

Parathyroid Hormone:

a) Hyper parathyroidism:

- Increased of PTH due to an adenoma of the parathyroid glands.

C/F:

- Pathologic fracture of bones due to increased mobilization of Ca

from bone resulting in osteitis fibrosa cystica.

- Large punched diet cystic area of bone.

1. Joint stiffness.

2. Urinary tract stones.

3. muscle weakness.

4. thirst.

5. Polyuria.

6. Anorexia.

7. Weight loss.

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 Dental findings.

Malocclusion seen due to definite drifting of teeth causing spacing (this

occurs as a result of increased loss of Ca +2 from the bone, there is an

absolute attempt to new bone formation and repair resulting in spacing).

Radiographically:

- Area of radiolucency seen in bone.

- Loss of lamina dura is present.

- Treatment removal of cause.

Hypoparathyroidism: Similar to hypocalcemia:

- This condition develop due to excision of the parathyroid glands.

- Characterized by a fall in the serum Ca levels and increased in the

serum inorganic phosphate levels.

C/F:

- Tingling and numbness in the fingers, face and toes.

- Extreme cases cramps in the hands and feet which are very painful.

- Spasm of muscles of respiration resulting in suffocation.

- Signs of tetany present, in infants, symptoms of tetany confused

with epilepsy, though there is no loss of consciousness.

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Dental findings;

- Aplasia/Hypoplasia of teeth seen when hypoparathyroidism

develops before teeth formation.

Parathyroid poisoning:

In rare cases, the PO4 level of body fluids rise rapidly when the kidneys cannot

excrete rapidly. Ca and PO4 get supersaturated and lead to metastatic deposition in

lungs, alveoli, kidneys, thyroid gland, gastric mucosa.

Elevation of blood Ca levels above 17mg/dl along with concurrent elevation of

PO4- death can occur in few days.

Osteoporosis:

Defined as a decrease in the absolute amount of bone, leading to fracture

following minimal trauma.

Common in old age (50 years onwards).

More in females.

Decreased matrix rather than poor bone calcification.

Management:

Adequate Ca+2 intake (1500mg).

Hormone replacement therapy in women.

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References:

1. Laureale Sherwood: From Cells to Systems

2. Harper’s Biochemistry 24th ed

3. Textbook of Medical Physiology 10th ed, Guyton & Hall

4. Essentials of Medical Physiology, k. Sembulingam & Prema

Sembulingam, 10th ed

5. Textbook of Medical Biochemistry, MN Chatterjee, Rana Shinde,5th ed

6. Concise Medical Physiology, Sujit K Chaudhuri, 2nd ed