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CALCIUM & PHOSPHATE
METABOLISM
PRESENTED BY:
ANU DUTTA
ANUMESH DAHAL
Contents:
 Introduction
 Distribution
 Daily requirements
 Dietary sources
 Functions
 Factors controlling absorption
 Hormonal control
 Other hormones affecting metabolism
 Clinical importance
 Conclusion
Objectives
 To know the role and daily
requirements of Calcium and
Phosphorous in body.
 To know the various factors
responsible for their absorption
 To know the hormonal influences on
calcium and phosphorus metabolism.
 To know the various abnormalities
related to hypo and hyper conditions
of phosphorus and calcium.
DEFINITION OF
METABOLISM
 Metabolism: is the biochemical
modification of chemical compounds
in living organisms and cells that
includes the biosynthesis of complex
organic molecules (anabolism) and
their breakdown (catabolism).
INTRODUCTION
 The minerals in foods do not contribute
directly to energy needs but are important as
body regulators and as essential constituents
in many vital substances within the body.
 About 25 elements have been found to be
essential, since a deficiency produces
specific
deficiency symptoms.
Principal Minerals include - Calcium, Phosphorous
Magnesium, Sodium, Potassium and Sulphur.
Calcium and phosphorous individually have their
own functions and together they are required for
the formation of hydroxyapatite and
physical strength of the skeletal tissue.
DISTRIBUTION
• Skeleton - 99%
• Muscle – 0.3%
• Other tissues – 0.7%
CALCIUM PHOSPAHATES
Skeleton – 90%
Intracellularly – 5%
Extracellularly - <0.03%
Distribution of Ca in ECF
CALCIUM PHOSPHATE
RATIO Calcium : Phosphate ratio normally is 2:1.
 Increase in plasma calcium levels causes
corresponding decrease in absorption of
phosphate.
 This ratio is always constant.
 The serum level of calcium is closely
regulated with normal total calcium of 9-10.5
mg/dL and normal ionized calcium of 4.5-5.6
mg/dL.
Serum Phosphate levels
 Children - 4 to 7 mg/dL
Daily Requirements
 Calcium:
Adults
Pregnancy
Lactating mother
Infants
Children
 Phosphates:
Adults
Pregnancy,
lactation & children
Infants
500-800mg
1500mg
2000mg
360mg
800mg
1200mg
240mg
800mg
Dietary Sources
Calcium:
- milk and milk
products
- eggs
- fish
- vegetables
- fruits (oranges)
- fortified bread
- nuts
- hard water
Phosphates:
- same as calcium
- present in high
amount
in cereals and pulses
- absent in hard water
Functions of Calcium
 Muscle contraction
Formation of bone and teeth
 Coagulation of blood
Nerve transmission:Integrity of
cell membrane by maintaining the
resting membrane potential of the cells
Release of certain hormones
 Major structural element in the
vertebrate skeleton (bones and teeth) in
the form of calcium phosphate
(Ca10(PO4)6(OH)2 known as
hydroxyapatatite
 Key component in the maintenance of
the cell structure
 Membrane rigidity, permeability and
viscosity are partly dependent on local
calcium concentrations
Functions of Phosphates
 Formation of bones.
 Like calcium, important component of teeth.
 Important constituent of cells.
 Forms energy rich bonds in ATP.
 Forms co-enzymes.
 Regulates blood and urinary pH.
 Forms organic molecules like DNA & RNA.
Absorption of Calcium
Calcium is taken through dietary sources as
calcium
phosphate, carbonate, tartarate and oxalate. It is
absorbed from the gastrointestinal tract in to blood
and
distributed to various parts of the body.
Two mechanisms have been proposed for the
absorption
of calcium by gut mucosa:
 Simple Diffusion.
 An active transport process, involving energy
and calcium pump.
 While passing through the kidney, large quantity
of
calcium is filtered in the glomerulus. From the
filtrate, 98 to 99% of calcium is reabsorbed in
the
renal tubules in to blood and only small
quantity is
excreted through urine. In the bone, the
calcium
may be deposited or resorbed depending upon
the
CALCIUM METABOLISM
Ca
Calcitonin
PTH Calcitriol
PTrP, GH,
Estrogen,GC,
Sex hormones
Role of calcium as intracellular
messenger
Factors controlling absorption
 Factors are classified into
1. Those acting on the mucosal cells
2. Those affecting the availability of
calcium and phosphates in the gut.
Factors acting on the mucosal
cells
 Vitamin D
 Pregnancy and growth
 PTH
VITAMIN-D
Calcitriol (1,25-DHCC) is the biologically
active form of Vitamin D
Synthesis of VITAMIN-D
Vitamin D
 Cholecalciferol / D3
 Ergocalciferol / D2
 Can be called as hormone as it is produced in the skin when
exposed to sunlight.
 Vitamin D has very little intrinsic biological activity.
Vitamin D itself is not a active substance, instead it must be first
converted through a succession of reaction in the liver and
the kidneys to the final active product 1, 25 di
hydroxycholecalciferol,
Daily requirement
 Adults – 2.5mg
 Lactating mother
Pregnancy
Adolescents
Infants
5mg
Dietary sources
 Cod liver oil
 Fish- Salmon
 Egg, liver
• Mean action of vitamin D is to increase the plasma level of
calcium.
• Increases intestinal Ca&P absorption.
Increases renal reabsorption of Calcium and
phosphate.
REGULATION OF SECRETION OF Vit.
• During later stages of pregnancy, greater amount of
calcium absorption is seen.
• 50% of this calcium is used for the development of fetal
skeleton and the rest is stored in the bones to act as a
reserve for lactation.
• This is due to the increased level of placental lactogen
and estrogen which stimulates increased hydroxylation of
vitamin D.
• In growth there is a increased level of growth hormone.
GH acts by increasing calcium absorption. It also
increases the renal excretion of calcium and phosphates.
Pregnancy and growth:
• 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.
Parathyroid Hormone:
Factors affecting availability of
Calcium and Phosphates in
gut.
 pH of the intestine
 Amount of dietary calcium and
phosphates
 Phytic acid and Phytates
 Oxalates
 Fats
 Proteins and amino acids
 Carbohydrates
pH of intestine:
• Acidic pH in the upper intestine (deodenum) increases
calcium absorption by keeping calcium salts in a soluble
state.
• In lower intestine since pH is more alkaline, calcium salts
undergoes precipitation
Amount of dietary calcium and
phosphates:
• Increased level of calcium and phosphate in diet
increases their absorption however up to a certain
limit.
• This is because the active process of their absorption
can bear with certain amounts of load beyond which
the excess would pass out into faeces
Phytic acid and phytates:
• They are present in oatmeal, meat and cereals and are
considered anti-calcifying factors as they combine with
calcium in the diet thus forming insoluble salts of calcium
Oxalates:
• They are present in spinach and rhubarb leaves. They
form oxalate precipitates with calcium present in the diet
thus decreasing their availability.
Fats:
• They combines with calcium and form insoluble calcium ,
thus decreasing calcium absorption.
Bile salts:
• They increases calcium absorption by promoting
metabolism of lipids.
•
Protein and aminoacids:
• High protein diet increases calcium absorption as protein
forms soluble complexes with calcium and keeps calcium
in a form that is easily absorbable.
Carbohydrates:
• Certain carbohydrates like lactose promotes calcium
absorption by creating the acidity in the gut as they
favours the growth of acid producing bacteria.
Hormonal Control of Calcium &
Phosphate metabolism
Three hormones regulate calcium and
phosphate metabolism.
 Vitamin D
 PTH
 Calcitonin
VITAMIN-D
Calcitriol acts at 3 different levels intestine,
kidney, bones
Action on Intestines:
It increases the intestinal absorption of calcium &
phosphate in the intestinal cells calcitriol binds with a
cytosolic receptor to form a calcitriol-receptor complex
This complex then approaches the nucleus and
interacts with a specific DNA leading to synthesis of
specific Ca binding protein.
This protein increases the Ca uptake by intestine.
Action on bone:
In the osteoblasts of bone calcitriol
stimulates Ca uptake for deposition as
capo4
Action on kidney:
It is involved in minimizing the excretion of
Ca & PO through kidney by decreasing their
excretion and enhancing reabsorption
Parathyroid Hormone
(PTH)
 Secreted by parathyroid gland
 Glands are four in number
 Present posterior to the thyroid gland
 Formed from third and fourth branchial pouches
 Combined weight of 130mg with each gland weighing
between 30-50mg.
 Histologically – two types of cells
Chief cells (forming PTH)
Oxyphilic cells (replaces the chief cells
stores hormone)
Actions of PTH
 The main function is to increase the level of
Ca in plasma within the critical range of 9
to11 mg.
 Parathormone inhibits renal phosphate
reabsorption in the proximal tubule and
therefore increases phosphate excretion
 Parathormone increases renal Calcium
reabsorption in the distal tubule, which also
increases the serum calcium.
 Net effect of PTH  ↑ serum calcium
↓ serum phosphate
Stimulation for PTH secretion
The stimulatory effect for PTH
secretion is low level of calcium in
plasma.
Maximum secretion occurs when
plasma calcium level falls below
7mg/dl.
When plasma calcium level increases
to 11mg/dl there is decreased
CALCITONIN
Minor regulator of calcium & phosphate
metabolism
Secreted by parafollicular cells or C-cells of
thyroid gland.
Also called as thyrocalcitonin.
Single chain polypeptide
Molecular weight 3400
Plasma concentration – 10-20ug/ml
Action of Calcitonin
 Net effect of calcitonin  decreases Serum Ca
 Target site
◦ Bone (osteoclasts)
decreased ability of osteoclasts to resorb bone
 Osteoclasts cells
◦ Lose their ruffled borders
◦ Undergo cytoskeletal rearrangement
◦ Decreased mobility
◦ Detach from bone
OTHER HORMONES on CALCIUM
METABOLISM
GROWTH HORMONE
 INSULIN
 TESTOSTERONE & OTHER
HORMONES
LACTOGEN & PROLACTIN
STEROIDS
THYROID HORMONES
Excretion of Calcium and Phosphorous
 Calcium is excreted in the urine, bile, and
digestive secretions.
 The renal threshold for serum ca is 10 mg/dl.
 70-90% of the calcium eliminated from the
body is excreted in the feces.
 The daily loss of calcium in sweat is about 15
mg.
Daily turnover rates of Ca in an adult are as follows:
Intake 1000mg.
Intestinal absorption 350mg
Secretion in GI juice 250mg
Net absorption over secretion 100mg
Loss in the faeces 200mg
Excretion in the urine 80-100mg
Phosphorous Excretion
 Phosphorous is excreted primarily through the
urine.
 Almost 2/3rd 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.
Increased serum Ca:
 1) Hyperparathyroidism.
 2) Hypervitaminosis (Vit. D).
 3) Multiple myeloma.
 4) Sarcoidosis.
 5) Thyrotoxicosis.
 6) Milk alkali syndrome.
 7) Infantile hypercalcemia
Decreased serum Ca:
 1) Renal failure.
 2) Hypoparathyroidism.
 3) Vit. D deficiency.
 4) Tetany.
 5) Malabsorption
syndrome.
SYMPTOMS OF CALCIUM -
PHOSPHORUS IMBALANCE
Frequent colds and 'flu
Sensitive to pain and noise
Signs of calcium deficiency
Tendency to low blood pressure
Blood is too acid
gingivitis
Red-rimmed eyes
Acute arthritic attacks
INCREASED SERUM PHOSPHATE LEVELS
Clinical Importance
Hypercalcemia
 Elevated serum calcium level up to 12- 15 mg/dl
Conditions leading to hypercalcemia
 Hyperparathyroidism
 Acute osteoporosis
 Thyrotoxicosis
 Vitamin D intoxication
Symptoms:
Polyuria,
dehydration,
confusion,
depression,
fatigue,
nausea/vomiting,
anorexia,
abdominal pain, and
renal calculi
Hypocalcaemia
 Decreased level of calcium in the blood
(<4mg/dl)
Conditions leading to hypocalcaemia
 Insufficient dietary calcium
 Hypoparathyroidism
 Insufficient vitamin D
 ↑ in calcitonin levels
Abnormal calcification
 Metastatic v/s Dystrophic
calcification
 Tetany (Carpopedal spasm)
Basic feature of tetany is uncontrolled,
painful, prolonged contraction (spasm)
of the voluntary muscles.
Chvostek’s sign
Contraction of ipsilateral facial muscles
when tapping facial nerve over the
angle of the mandible.
Erbs sign
◦ Hyperexitability of muscles to electrical stimulation
• Trousseau’s sign
• Spasm of the muscles of the upper extremity causing
flexion of wrist and thumb and extension of fingers.
• Clinically can be produced by applying pressure with
sphygmomanometer cuff on the upper arm.
Vitamin D deficiency
 Rickets
◦ Occurs in children between 6
months to 2 years of age.
◦ Affects long bones
◦ Lack of calcium causes failure of
mineralization resulting into
formation of cartilagenous form
of bone.
◦ Most critical area that gets
affected is the center
endochondral ossification at the
epiphyseal plates.
Dental findings in Ricketts
 Developmental anomalies of enamel and
dentin
 Delayed eruption
 Misalignment of teeth
 Increase caries index
 Wide predentin zone and more interglobular
dentin
Treatment
Daily administration of 1000 – 4000 units of vit.D.
Osteomalacia v/s Osteoporosis
Hyperparathyroidism
May be Primary or Secondary.
Primary hyperparathyroidism
 In Primary form, a primary abnormality of the
parathyroid glands causes inappropriate, excess
PTH secretion.
 Caused mainly by an adenoma of parathyroid.
Secondary Hyperparathyroidism
 In Secondary form, high levels of PTH occur
as a
compensation rather than as a primary
abnormality of the parathyroid glands.
 It can be caused by Vitamin D deficiency or
chronic renal disease.
Hypoparathyroidism
 Decrease level of PTH
 Due to
◦ Surgical removal of parathyroid gland
◦ Congenital absence of the gland
◦ Atrophy of the gland
 Diagnosis
◦ Decrease plasma calcium level & increase plasma
phosphate level
Oral Manifestations:
Dryness of the mucous membranes,
Angular cheilitis
Circumoral parasthesia
Pseudohypoparathyroidism
 is the result of defective G protein in kidney and
bone, which causes end-organ resistance to PT
 there is hypocalcemia and hyperphosphatemia th
is
not correctable by administration of exogenous
PTH.
 circulating endogenous PTH levels are elevated.
• Increased intake Diet containing Vit-D
• Increased release of P from cells (DM, Acidaemia,
Starvation)
• Increased release of P from bone (malignancy, Renal
failure, Increased PTH)
• Decreased excretion (Renal failure, Hyperparathyroidism,
Increased growth hormone)
• Phosphate trapping
• Respiratory insufficiency
• Erythrocyte dysfunction
• Nervous Dysfunction
• Leukocyte Dysfunction
• Metabolic acidosis
• Decreased Intake (Starvation, Malabsorption, Vomiting)
• Increased cell uptake (High dietary carbohydrate, Liver
disease)
• Increased Excretion (Diuretics, Hypomagnesaemia,
Increased PTH)
HYPOPHOSPHATASIA
The basic disorder is a deficiency of the enzyme
alkaline phosphatase in serum or tissues and
excretion of phosphoethanolamine in the urine.
.
Oral manifestations:
Loosening and premature loss of deciduous teeth,
chiefly the incisors.
PSEUDOHYPOPHOSPHATASIA:
A disease resembling classic hypophosphatasia
but with
a normal serum alkaline phosphatase level.
Patients exhibit osteopathy of the long bones and
skull,
premature loss of deciduous teeth, hypotonia,
hypercalcemia and phosphoethanolaminauria.
• It has often been supposed that a low intake
of calcium, or phosphorous, or both might lead
to poor calcification of teeth and possibly,
therefore, to an increased risk of dental
caries.
• the calcification of the teeth could be affected
if calcium was very low in the diet.
• deficiencies in calcium and phosphate intake
do not affect tooth calcification they do
reduce that of bone, and they result in
mobilization of calcium from already formed
bone.
• In pregnancy, when the dietary need of the
mother for calcium and phosphate are
increased by the demands imposed by the
growing fetus, there is mobilization of bone
calcium if the dietary supply is insufficient.
Conclusion
Disturbances in calcium and phosphate intake,
excretion and transcellular shift result in deranged
metabolism accounting for abnormal serum levels.
As a result of the essential role played by these
minerals in intra and extracellular metabolism, the
clinical manifestations of related disease states are
extensive.
Thus, an understanding of the basic mechanism of
calcium, phosphate metabolism and pathophysiology
of various related disorders is helpful in guiding
therapeutic decisions.
References
 Textbook of Biochemistry by U.
Satyanarayana, second edition.
 Essentials of Medical Physiology by K.
Sambulingam,
third edition.
 Textbook of Medical Physiology by Guyton and
Hall, tenth edition.
 Shafer’s textbook of oral pathology, Fifth
edition
 Burkets oral medicine 11th edition

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Calcium & Phosphate Metabolism

  • 1. CALCIUM & PHOSPHATE METABOLISM PRESENTED BY: ANU DUTTA ANUMESH DAHAL
  • 2. Contents:  Introduction  Distribution  Daily requirements  Dietary sources  Functions  Factors controlling absorption  Hormonal control  Other hormones affecting metabolism  Clinical importance  Conclusion
  • 3. Objectives  To know the role and daily requirements of Calcium and Phosphorous in body.  To know the various factors responsible for their absorption  To know the hormonal influences on calcium and phosphorus metabolism.  To know the various abnormalities related to hypo and hyper conditions of phosphorus and calcium.
  • 4. DEFINITION OF METABOLISM  Metabolism: is the biochemical modification of chemical compounds in living organisms and cells that includes the biosynthesis of complex organic molecules (anabolism) and their breakdown (catabolism).
  • 5. INTRODUCTION  The minerals in foods do not contribute directly to energy needs but are important as body regulators and as essential constituents in many vital substances within the body.  About 25 elements have been found to be essential, since a deficiency produces specific deficiency symptoms.
  • 6. Principal Minerals include - Calcium, Phosphorous Magnesium, Sodium, Potassium and Sulphur. Calcium and phosphorous individually have their own functions and together they are required for the formation of hydroxyapatite and physical strength of the skeletal tissue.
  • 7. DISTRIBUTION • Skeleton - 99% • Muscle – 0.3% • Other tissues – 0.7% CALCIUM PHOSPAHATES Skeleton – 90% Intracellularly – 5% Extracellularly - <0.03%
  • 9. CALCIUM PHOSPHATE RATIO Calcium : Phosphate ratio normally is 2:1.  Increase in plasma calcium levels causes corresponding decrease in absorption of phosphate.  This ratio is always constant.  The serum level of calcium is closely regulated with normal total calcium of 9-10.5 mg/dL and normal ionized calcium of 4.5-5.6 mg/dL. Serum Phosphate levels  Children - 4 to 7 mg/dL
  • 10. Daily Requirements  Calcium: Adults Pregnancy Lactating mother Infants Children  Phosphates: Adults Pregnancy, lactation & children Infants 500-800mg 1500mg 2000mg 360mg 800mg 1200mg 240mg 800mg
  • 11. Dietary Sources Calcium: - milk and milk products - eggs - fish - vegetables - fruits (oranges) - fortified bread - nuts - hard water Phosphates: - same as calcium - present in high amount in cereals and pulses - absent in hard water
  • 12. Functions of Calcium  Muscle contraction Formation of bone and teeth  Coagulation of blood Nerve transmission:Integrity of cell membrane by maintaining the resting membrane potential of the cells Release of certain hormones
  • 13.  Major structural element in the vertebrate skeleton (bones and teeth) in the form of calcium phosphate (Ca10(PO4)6(OH)2 known as hydroxyapatatite  Key component in the maintenance of the cell structure  Membrane rigidity, permeability and viscosity are partly dependent on local calcium concentrations
  • 14.
  • 15. Functions of Phosphates  Formation of bones.  Like calcium, important component of teeth.  Important constituent of cells.  Forms energy rich bonds in ATP.  Forms co-enzymes.  Regulates blood and urinary pH.  Forms organic molecules like DNA & RNA.
  • 16. Absorption of Calcium Calcium is taken through dietary sources as calcium phosphate, carbonate, tartarate and oxalate. It is absorbed from the gastrointestinal tract in to blood and distributed to various parts of the body. Two mechanisms have been proposed for the absorption of calcium by gut mucosa:  Simple Diffusion.  An active transport process, involving energy and calcium pump.
  • 17.  While passing through the kidney, large quantity of calcium is filtered in the glomerulus. From the filtrate, 98 to 99% of calcium is reabsorbed in the renal tubules in to blood and only small quantity is excreted through urine. In the bone, the calcium may be deposited or resorbed depending upon the
  • 19. Role of calcium as intracellular messenger
  • 20. Factors controlling absorption  Factors are classified into 1. Those acting on the mucosal cells 2. Those affecting the availability of calcium and phosphates in the gut.
  • 21. Factors acting on the mucosal cells  Vitamin D  Pregnancy and growth  PTH
  • 22. VITAMIN-D Calcitriol (1,25-DHCC) is the biologically active form of Vitamin D Synthesis of VITAMIN-D
  • 23. Vitamin D  Cholecalciferol / D3  Ergocalciferol / D2  Can be called as hormone as it is produced in the skin when exposed to sunlight.  Vitamin D has very little intrinsic biological activity. Vitamin D itself is not a active substance, instead it must be first converted through a succession of reaction in the liver and the kidneys to the final active product 1, 25 di hydroxycholecalciferol,
  • 24. Daily requirement  Adults – 2.5mg  Lactating mother Pregnancy Adolescents Infants 5mg
  • 25. Dietary sources  Cod liver oil  Fish- Salmon  Egg, liver • Mean action of vitamin D is to increase the plasma level of calcium. • Increases intestinal Ca&P absorption. Increases renal reabsorption of Calcium and phosphate.
  • 27. • During later stages of pregnancy, greater amount of calcium absorption is seen. • 50% of this calcium is used for the development of fetal skeleton and the rest is stored in the bones to act as a reserve for lactation. • This is due to the increased level of placental lactogen and estrogen which stimulates increased hydroxylation of vitamin D. • In growth there is a increased level of growth hormone. GH acts by increasing calcium absorption. It also increases the renal excretion of calcium and phosphates. Pregnancy and growth:
  • 28. • 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. Parathyroid Hormone:
  • 29. Factors affecting availability of Calcium and Phosphates in gut.  pH of the intestine  Amount of dietary calcium and phosphates  Phytic acid and Phytates  Oxalates  Fats  Proteins and amino acids  Carbohydrates
  • 30. pH of intestine: • Acidic pH in the upper intestine (deodenum) increases calcium absorption by keeping calcium salts in a soluble state. • In lower intestine since pH is more alkaline, calcium salts undergoes precipitation
  • 31. Amount of dietary calcium and phosphates: • Increased level of calcium and phosphate in diet increases their absorption however up to a certain limit. • This is because the active process of their absorption can bear with certain amounts of load beyond which the excess would pass out into faeces
  • 32. Phytic acid and phytates: • They are present in oatmeal, meat and cereals and are considered anti-calcifying factors as they combine with calcium in the diet thus forming insoluble salts of calcium Oxalates: • They are present in spinach and rhubarb leaves. They form oxalate precipitates with calcium present in the diet thus decreasing their availability. Fats: • They combines with calcium and form insoluble calcium , thus decreasing calcium absorption.
  • 33. Bile salts: • They increases calcium absorption by promoting metabolism of lipids. • Protein and aminoacids: • High protein diet increases calcium absorption as protein forms soluble complexes with calcium and keeps calcium in a form that is easily absorbable. Carbohydrates: • Certain carbohydrates like lactose promotes calcium absorption by creating the acidity in the gut as they favours the growth of acid producing bacteria.
  • 34. Hormonal Control of Calcium & Phosphate metabolism Three hormones regulate calcium and phosphate metabolism.  Vitamin D  PTH  Calcitonin
  • 35. VITAMIN-D Calcitriol acts at 3 different levels intestine, kidney, bones Action on Intestines: It increases the intestinal absorption of calcium & phosphate in the intestinal cells calcitriol binds with a cytosolic receptor to form a calcitriol-receptor complex This complex then approaches the nucleus and interacts with a specific DNA leading to synthesis of specific Ca binding protein. This protein increases the Ca uptake by intestine.
  • 36. Action on bone: In the osteoblasts of bone calcitriol stimulates Ca uptake for deposition as capo4 Action on kidney: It is involved in minimizing the excretion of Ca & PO through kidney by decreasing their excretion and enhancing reabsorption
  • 37. Parathyroid Hormone (PTH)  Secreted by parathyroid gland  Glands are four in number  Present posterior to the thyroid gland  Formed from third and fourth branchial pouches  Combined weight of 130mg with each gland weighing between 30-50mg.  Histologically – two types of cells Chief cells (forming PTH) Oxyphilic cells (replaces the chief cells stores hormone)
  • 38.
  • 39. Actions of PTH  The main function is to increase the level of Ca in plasma within the critical range of 9 to11 mg.  Parathormone inhibits renal phosphate reabsorption in the proximal tubule and therefore increases phosphate excretion  Parathormone increases renal Calcium reabsorption in the distal tubule, which also increases the serum calcium.  Net effect of PTH  ↑ serum calcium ↓ serum phosphate
  • 40. Stimulation for PTH secretion The stimulatory effect for PTH secretion is low level of calcium in plasma. Maximum secretion occurs when plasma calcium level falls below 7mg/dl. When plasma calcium level increases to 11mg/dl there is decreased
  • 41. CALCITONIN Minor regulator of calcium & phosphate metabolism Secreted by parafollicular cells or C-cells of thyroid gland. Also called as thyrocalcitonin. Single chain polypeptide Molecular weight 3400 Plasma concentration – 10-20ug/ml
  • 42. Action of Calcitonin  Net effect of calcitonin  decreases Serum Ca  Target site ◦ Bone (osteoclasts) decreased ability of osteoclasts to resorb bone  Osteoclasts cells ◦ Lose their ruffled borders ◦ Undergo cytoskeletal rearrangement ◦ Decreased mobility ◦ Detach from bone
  • 43. OTHER HORMONES on CALCIUM METABOLISM GROWTH HORMONE  INSULIN  TESTOSTERONE & OTHER HORMONES LACTOGEN & PROLACTIN STEROIDS THYROID HORMONES
  • 44. Excretion of Calcium and Phosphorous  Calcium is excreted in the urine, bile, and digestive secretions.  The renal threshold for serum ca is 10 mg/dl.  70-90% of the calcium eliminated from the body is excreted in the feces.  The daily loss of calcium in sweat is about 15 mg.
  • 45. Daily turnover rates of Ca in an adult are as follows: Intake 1000mg. Intestinal absorption 350mg Secretion in GI juice 250mg Net absorption over secretion 100mg Loss in the faeces 200mg Excretion in the urine 80-100mg
  • 46. Phosphorous Excretion  Phosphorous is excreted primarily through the urine.  Almost 2/3rd 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.
  • 47. Increased serum Ca:  1) Hyperparathyroidism.  2) Hypervitaminosis (Vit. D).  3) Multiple myeloma.  4) Sarcoidosis.  5) Thyrotoxicosis.  6) Milk alkali syndrome.  7) Infantile hypercalcemia Decreased serum Ca:  1) Renal failure.  2) Hypoparathyroidism.  3) Vit. D deficiency.  4) Tetany.  5) Malabsorption syndrome. SYMPTOMS OF CALCIUM - PHOSPHORUS IMBALANCE
  • 48. Frequent colds and 'flu Sensitive to pain and noise Signs of calcium deficiency Tendency to low blood pressure Blood is too acid gingivitis Red-rimmed eyes Acute arthritic attacks INCREASED SERUM PHOSPHATE LEVELS
  • 49. Clinical Importance Hypercalcemia  Elevated serum calcium level up to 12- 15 mg/dl Conditions leading to hypercalcemia  Hyperparathyroidism  Acute osteoporosis  Thyrotoxicosis  Vitamin D intoxication
  • 51. Hypocalcaemia  Decreased level of calcium in the blood (<4mg/dl) Conditions leading to hypocalcaemia  Insufficient dietary calcium  Hypoparathyroidism  Insufficient vitamin D  ↑ in calcitonin levels
  • 52. Abnormal calcification  Metastatic v/s Dystrophic calcification
  • 53.  Tetany (Carpopedal spasm) Basic feature of tetany is uncontrolled, painful, prolonged contraction (spasm) of the voluntary muscles. Chvostek’s sign Contraction of ipsilateral facial muscles when tapping facial nerve over the angle of the mandible. Erbs sign ◦ Hyperexitability of muscles to electrical stimulation
  • 54. • Trousseau’s sign • Spasm of the muscles of the upper extremity causing flexion of wrist and thumb and extension of fingers. • Clinically can be produced by applying pressure with sphygmomanometer cuff on the upper arm.
  • 55. Vitamin D deficiency  Rickets ◦ Occurs in children between 6 months to 2 years of age. ◦ Affects long bones ◦ Lack of calcium causes failure of mineralization resulting into formation of cartilagenous form of bone. ◦ Most critical area that gets affected is the center endochondral ossification at the epiphyseal plates.
  • 56. Dental findings in Ricketts  Developmental anomalies of enamel and dentin  Delayed eruption  Misalignment of teeth  Increase caries index  Wide predentin zone and more interglobular dentin Treatment Daily administration of 1000 – 4000 units of vit.D.
  • 58. Hyperparathyroidism May be Primary or Secondary. Primary hyperparathyroidism  In Primary form, a primary abnormality of the parathyroid glands causes inappropriate, excess PTH secretion.  Caused mainly by an adenoma of parathyroid.
  • 59. Secondary Hyperparathyroidism  In Secondary form, high levels of PTH occur as a compensation rather than as a primary abnormality of the parathyroid glands.  It can be caused by Vitamin D deficiency or chronic renal disease.
  • 60. Hypoparathyroidism  Decrease level of PTH  Due to ◦ Surgical removal of parathyroid gland ◦ Congenital absence of the gland ◦ Atrophy of the gland  Diagnosis ◦ Decrease plasma calcium level & increase plasma phosphate level
  • 61. Oral Manifestations: Dryness of the mucous membranes, Angular cheilitis Circumoral parasthesia
  • 62. Pseudohypoparathyroidism  is the result of defective G protein in kidney and bone, which causes end-organ resistance to PT  there is hypocalcemia and hyperphosphatemia th is not correctable by administration of exogenous PTH.  circulating endogenous PTH levels are elevated.
  • 63. • Increased intake Diet containing Vit-D • Increased release of P from cells (DM, Acidaemia, Starvation) • Increased release of P from bone (malignancy, Renal failure, Increased PTH) • Decreased excretion (Renal failure, Hyperparathyroidism, Increased growth hormone)
  • 64. • Phosphate trapping • Respiratory insufficiency • Erythrocyte dysfunction • Nervous Dysfunction • Leukocyte Dysfunction • Metabolic acidosis
  • 65. • Decreased Intake (Starvation, Malabsorption, Vomiting) • Increased cell uptake (High dietary carbohydrate, Liver disease) • Increased Excretion (Diuretics, Hypomagnesaemia, Increased PTH)
  • 66. HYPOPHOSPHATASIA The basic disorder is a deficiency of the enzyme alkaline phosphatase in serum or tissues and excretion of phosphoethanolamine in the urine. . Oral manifestations: Loosening and premature loss of deciduous teeth, chiefly the incisors.
  • 67. PSEUDOHYPOPHOSPHATASIA: A disease resembling classic hypophosphatasia but with a normal serum alkaline phosphatase level. Patients exhibit osteopathy of the long bones and skull, premature loss of deciduous teeth, hypotonia, hypercalcemia and phosphoethanolaminauria.
  • 68. • It has often been supposed that a low intake of calcium, or phosphorous, or both might lead to poor calcification of teeth and possibly, therefore, to an increased risk of dental caries. • the calcification of the teeth could be affected if calcium was very low in the diet.
  • 69. • deficiencies in calcium and phosphate intake do not affect tooth calcification they do reduce that of bone, and they result in mobilization of calcium from already formed bone. • In pregnancy, when the dietary need of the mother for calcium and phosphate are increased by the demands imposed by the growing fetus, there is mobilization of bone calcium if the dietary supply is insufficient.
  • 70. Conclusion Disturbances in calcium and phosphate intake, excretion and transcellular shift result in deranged metabolism accounting for abnormal serum levels. As a result of the essential role played by these minerals in intra and extracellular metabolism, the clinical manifestations of related disease states are extensive. Thus, an understanding of the basic mechanism of calcium, phosphate metabolism and pathophysiology of various related disorders is helpful in guiding therapeutic decisions.
  • 71. References  Textbook of Biochemistry by U. Satyanarayana, second edition.  Essentials of Medical Physiology by K. Sambulingam, third edition.  Textbook of Medical Physiology by Guyton and Hall, tenth edition.  Shafer’s textbook of oral pathology, Fifth edition  Burkets oral medicine 11th edition

Editor's Notes

  1. As dentist it is vital for us to have a complete understanding of the general metabolism of Calcium and phosphorus as it is these minerals that help in the formation and the maintenance of the teeth and their supporting bony structure
  2. Macro-elements Calcium, Phosphorous, Sodium, Potassium, Chloride, Sulphur Micro-elements Iron, Iodine, Copper, Cobalt, Zinc, Fluoride,
  3. In growth there is a increased level of growth hormone. GH acts by increasing calcium absorption. It also increases the renal excretion of calcium and phosphates.
  4. Site of release ??
  5. Brief hints about positive and negative cacium balance!!!
  6. Calcitonin is physiological antagonist of PTH with respect to calcium whereas with respect to phosphate it has same effect as PTH ie decreases plasma phosphate level
  7. Symptoms are Irritability, muscle cramps,depression, bronchospasm, and seizures
  8. Skeletal deformities!!!
  9. It is different from osteomalacia and rickets because it results from diminished organic bone matrix rather than from poor bone calcification
  10. Other manifestations can be like Enamel hypoplasia and dental dysplasia,Disturbances in tooth eruption ,Root defects etc.
  11. vinaymarla85@gmail.com